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'''Dementia''' is "progressive decline in two or more cognitive domains that is severe enough to interfere with the performance of everyday activities."<ref name="pmid12614094">{{cite journal |author=Karlawish, J. & Clark, C. |title=Diagnostic evaluation of elderly patients with mild memory problems |journal=Ann Intern Med |volume=138 |issue=5 |pages=411-9 |year=2003 |pmid=12614094 | url=http://www.annals.org/cgi/content/full/138/5/411}}</ref>
'''Dementia''' is a syndrome associated with many neurodegenerative diseases, characterized by a general decline in cognitive abilities that affects a person's ability to perform everyday activities.  Dementia may involve problems with memory, thinking, behavior, and motor control. Aside from memory impairment and a disruption in thought patterns, the most common symptoms of dementia include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than might be caused by the normal aging process.  Dementia is currently the seventh leading cause of death worldwide and has 10 million new cases reported every year (approximately one every three seconds).
 
==History==
 
Until the end of the 19th century, dementia was a much broader clinical concept. It included mental illness and any type of psychosocial incapacity, including reversible conditions. Dementia at this time simply referred to anyone who had lost the ability to reason, and was applied equally to psychosis, "organic" diseases like syphilis that can destroy the brain, and to the dementia associated with old age, which was attributed to "hardening of the arteries".
 
In Roman times, philosopher Emperor Marcus Aurelius, who lived from 161 to 180 C.E., feared falling into a state of dementia more than he feared death. He wrote:
<poem style="border: 2px solid #d6d2c5; background-color: #f9f4e6; padding: 1em; width: 80%">
"...if we live longer, there is no guarantee that our mind will likewise retain that power to comprehend and study the world which contributes to our experience of things divine and human. If dementia sets in, there will be no failure of such faculties as breathing, feeding, imagination, desire: before these go, the earlier extinction is of one's proper use of oneself, one's accurate assessment of the gradations of duty, one's ability to analyse impressions, one's understanding of whether the time has come to leave this life - these and all other matters which wholly depend on trained calculation. So we must have a sense of urgency, not only for the ever closer approach of death, but also because our comprehension of the world and our ability to pay proper attention will fade before we do."  --''Meditations'' 3:1, Marcus Aurelius
</poem>
 
==Possible causes==
Various diseases and injuries to the brain, such as stroke, can give rise to dementia. However, the most common cause is Alzheimer's disease, a neurodegenerative disorder. The ''Diagnostic and Statistical Manual of Mental Disorders'', Fifth Edition (DSM-5), has re-described dementia as a mild or major neurocognitive disorder with varying degrees of severity and many causative subtypes. The International Classification of Diseases (ICD-11) also classifies dementia as a neurocognitive disorder (NCD) with many forms or subclasses. Dementia is listed as an acquired brain syndrome, marked by a decline in cognitive function, and is contrasted with neurodevelopmental disorders. It is also described as a spectrum of disorders with causative subtypes of dementia based on a known disorder, such as Parkinson's disease for Parkinson's disease dementia, Huntington's disease for Huntington's disease dementia, vascular disease for vascular dementia, HIV infection causing HIV dementia, frontotemporal lobar degeneration for frontotemporal dementia, Lewy body disease for dementia with Lewy bodies, and prion diseases.<ref>Wilson H, Pagano G, Politis M (March 2019). "Dementia spectrum disorders: lessons learnt from decades with PET research". J Neural Transm (Vienna). 126(3): 233–251. [[doi:10.1007/s00702-019-01975-4]]. PMC 6449308. PMID 30762136.</ref> Subtypes of neurodegenerative dementias may also be based on the underlying pathology of misfolded proteins, such as synucleinopathies and tauopathies. The coexistence of more than one type of dementia is known as mixed dementia.
 
Many neurocognitive disorders may be caused by another medical condition or disorder, including brain tumors and subdural hematoma, endocrine disorders such as hypothyroidism and hypoglycemia, nutritional deficiencies including of thiamine and niacin, infections, immune disorders, liver or kidney failure, metabolic disorders such as Kufs disease, some leukodystrophies, and neurological disorders such as epilepsy and multiple sclerosis. Some of the neurocognitive deficits may sometimes show improvement with treatment of the causative medical condition.
 
Decades of published scientific research strongly implicate long-term exposure to low levels of aluminum in the development of Alzheimer's disease. This dementia was completely unknown to medicine before the proliferation of aluminum throughout industrialized societies beginning in the late 19th century.
 
==Signs and symptoms==
 
The signs and symptoms of dementia are termed as the neuropsychiatric symptoms—also known as the behavioral and psychological symptoms—of dementia. The behavioral symptoms can include agitation, restlessness, inappropriate behavior, sexual disinhibition, and verbal or physical aggression. These symptoms may result from impairments in cognitive inhibition. The psychological symptoms can include depression, hallucinations (most often visual), delusions, apathy, and anxiety. The most commonly affected areas of brain function include memory, language, attention, problem solving, and visuospatial function affecting perception and orientation. The symptoms progress at a continuous rate over several stages, and they vary across the dementia subtypes. Most types of dementia are slowly progressive with some deterioration of the brain well established before signs of the disorder become apparent. There are often other conditions present, such as high blood pressure or diabetes, and there can sometimes be as many as four of these comorbidities.
 
Signs of dementia include getting lost in a familiar neighborhood, using unusual words to refer to familiar objects, forgetting the name of a close family member or friend, forgetting old memories, and being unable to complete tasks independently, such as paying bills or balancing a checkbook.
 
People with dementia are more likely to have problems with incontinence than those of a comparable age without dementia; they are three times more likely to have urinary incontinence and four times more likely to have fecal incontinence.
 
==Stages==
 
The course of dementia is often described in four stages – pre-dementia, early, middle, and late, that show a pattern of progressive cognitive and functional impairment. More detailed descriptions can be arrived at by the use of numeric scales. These scales include the Global Deterioration Scale for Assessment of Primary Degenerative Dementia (GDS or Reisberg Scale), the Functional Assessment Staging Test (FAST), and the Clinical Dementia Rating (CDR). Using the GDS, which more accurately identifies each stage of the disease progression, a more detailed course is described in seven stages – two of which are broken down further into five and six degrees. Stage 7(f) is the final stage.


Deficits in cognitive function contribute to impaired functional status.<ref name="pmid17827410">{{cite journal |author=Royall DR, Lauterbach EC, Kaufer D, Malloy P, Coburn KL, Black KJ |title=The cognitive correlates of functional status: a review from the Committee on Research of the American Neuropsychiatric Association |journal=The Journal of neuropsychiatry and clinical neurosciences |volume=19 |issue=3 |pages=249–65 |year=2007 |pmid=17827410 |doi=10.1176/appi.neuropsych.19.3.249}}</ref> The deficits in the domains of cognitive function are<ref name="pmid17551132">{{cite journal |author=Holsinger T, Deveau J, Boustani M, Williams JW |title=Does this patient have dementia? |journal=JAMA |volume=297 |issue=21 |pages=2391–404 |year=2007 |pmid=17551132 |doi=10.1001/jama.297.21.2391}}</ref>:
* Agnosia - "Failure to recognize or identify objects despite intact sensory function"<ref name="pmid17551132"/>
* Aphasia - "Deterioration of language function"<ref name="pmid17551132"/>
* Apraxia - "Impaired ability to execute motor activities despite intact motor abilities, sensory function, and comprehension of the required task"<ref name="pmid17551132"/>
* Disturbance in executive functioning - "The ability to think abstractly and to plan, initiate, sequence, monitor, and stop complex behavior"<ref name="pmid17551132"/>
==Classification==
==Classification==
Vascular dementia can affect both cortical and subcortial locations.
Vascular dementia can affect both cortical and subcortial locations.
Line 19: Line 41:


===Subcortical dementias===
===Subcortical dementias===
Among the many causes of subcortical dementia, common causes are:
Among the many causes of subcortical dementia, common causes are [[Parkinson's disease]], vitamin B12 deficiency, and some vascular dementias.
* [[Parkinson's disease]]  
* [[Vitamin B12 deficiency]]
* Some [[vascular dementia]]s


==Epidemiology==
==Epidemiology==
22.2% of individuals in the United States age 71 years or older have cognitive impairment without dementia (Dementia Severity Rating Scale score of 6 to 11). 12% of these patients progress to dementia annually. Progression is more common among patients with subtypes of prodromal Alzheimer disease and cerebrovascular disease.<ref name="pmid18347351">{{cite journal |author=Plassman BL, Langa KM, Fisher GG, ''et al'' |title=Prevalence of cognitive impairment without dementia in the United States |journal=Ann. Intern. Med. |volume=148 |issue=6 |pages=427–34 |year=2008 |month=March |pmid=18347351 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=18347351 |issn=}}</ref>
The number of cases of dementia worldwide in 2021 was estimated at 55 million, with close to 10 million new cases each year.<ref>"Dementia". [https://www.who.int/news-room/fact-sheets/detail/dementia World Health Organization]. Retrieved October 29, 2024.</ref> According to a report by the World Health Organization, "In 2021, Alzheimer’s disease and other forms of dementia ranked as the seventh leading cause of death, killing 1.8 million lives." By 2050, the number of people living with dementia is estimated to be over 150 million globally. Around 7% of people over the age of 65 have dementia, with slightly higher rates (up to 10% of those over 65) in places with relatively high life expectancy. In the United States, an estimated 40% of those over the age of 85 years old will eventually develop Alzheimer's dementia. The prevalence of dementia differs in different world regions, ranging from 4.7% in Central Europe to 8.7% in North Africa/Middle East; the prevalence in other regions is estimated to be between 5.6 and 7.6%. The number of people living with dementia is estimated to double every 20 years. In 2016 dementia resulted in about 2.4 million deaths, up from 0.8 million in 1990.


===Risk factors===
The annual incidence of dementia diagnosis is nearly 10 million worldwide. Almost half of new dementia cases occur in Asia, followed by Europe (25%), the Americas (18%), and Africa (8%). The incidence of dementia increases exponentially with age, doubling with every 6.3-year increase in age.<ref>[https://www.alzint.org/u/WorldAlzheimerReport2015.pdf Alzheimer's Disease International (September 2015). "World Alzheimer Report 2015" (PDF)]. Retrieved October 29, 2024.</ref> Rates are slightly higher in women than men at ages 65 and greater. The disease trajectory is varied and the median time from diagnosis to death depends strongly on age at diagnosis, from 6.7 years for people diagnosed aged 60–69 to 1.9 years for people diagnosed at 90 or older.
Repeated episodes of hypoglycemia are associated with dementia.<ref name="pmid19366776">{{cite journal |author=Whitmer RA, Karter AJ, Yaffe K, Quesenberry CP, Selby JV |title=Hypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus |journal=JAMA |volume=301 |issue=15 |pages=1565–72 |year=2009 |month=April |pmid=19366776 |doi=10.1001/jama.2009.460 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=19366776 |issn=}}</ref>


Hypoxia from sleep disordered breathing such as [[sleep apnea]] may increase risk.<ref>{{Cite journal
Dementia impacts not only individuals with dementia, but also their carers and the wider society. Among people aged 60 years and over, dementia is ranked the ninth most burdensome condition according to the 2010 Global Burden of Disease (GBD) estimates. The global costs of dementia was around U.S. $818 billion in 2015, a 35.4% increase from U.S. $604 billion in 2010.
| doi = 10.1001/jama.2011.1115
 
| volume = 306
A new 2024 study reveals that deaths from dementia in the U.S. have tripled in the past 21 years, rising from around 150,000 in 1999 to over 450,000 in 2020; the likelihood of dying from dementia increased across all demographic groups studied.
| issue = 6
| pages = 613 -619
| last = Yaffe
| first = Kristine
| coauthors = Alison M. Laffan, Stephanie Litwack Harrison, Susan Redline, Adam P. Spira, Kristine E. Ensrud, Sonia Ancoli-Israel, Katie L. Stone
| title = Sleep-Disordered Breathing, Hypoxia, and Risk of Mild Cognitive Impairment and Dementia in Older Women
| journal = JAMA: The Journal of the American Medical Association
| accessdate = 2011-08-11
| date = 2011
| url = http://jama.ama-assn.org/content/306/6/613.abstract
}}</ref>


==Diagnosis==
==Diagnosis==
Studies on diagnosing dementia are compromised by the lack of a true reference standard for comparison.<ref name="pmid9385127">{{cite journal |author=Erkinjuntti T, Ostbye T, Steenhuis R, Hachinski V |title=The effect of different diagnostic criteria on the prevalence of dementia |journal=N. Engl. J. Med. |volume=337 |issue=23 |pages=1667–74 |year=1997 |month=December |pmid=9385127 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9385127&promo=ONFLNS19 |issn=}}</ref><ref>Rockwood K et al. [http://dx.doi.org/10.1016/j.jalz.2007.07.014 Toward a revision of criteria for the dementias]. Alzheimer's and Dementia 3 (4), 428 (2007) {{doi|10.1016/j.jalz.2007.07.014}}</ref>
Symptoms are similar across dementia types, and it is difficult to diagnose by symptoms alone. Diagnosis may be aided by brain scanning techniques. In many cases, the diagnosis requires a brain biopsy to become final, but this is rarely recommended (though it can be performed at autopsy). In those who are getting older, general screening for cognitive impairment using cognitive testing or early diagnosis of dementia has not been shown to improve outcomes. However, screening exams are useful in 65+ persons with memory or function complaints.


A number of [[systematic review]]s, including ones by the [http://www.ahrq.gov/clinic/uspstfix.htm U.S. Preventive Services Task Force (USPSTF)]<ref name="pmid12779304">{{cite journal |author=Boustani, M.; Peterson, B.; Hanson, L.; Harris, R.; & Lohr, K. |title=Screening for dementia in primary care: a summary of the evidence for the U.S. Preventive Services Task Force |journal=Ann Intern Med |volume=138 |issue=11 |pages=927-37 |year=2003 |pmid=12779304 | url=http://www.annals.org/cgi/content/full/138/11/927}}</ref>, [http://www.sgim.org/clinexam-rce.cfm Rational Clinical Examination]<ref name="pmid17551132">{{cite journal |author=Holsinger T, Deveau J, Boustani M, Williams JW |title=Does this patient have dementia? |journal=JAMA |volume=297 |issue=21 |pages=2391–404 |year=2007 |pmid=17551132 |doi=10.1001/jama.297.21.2391}}</ref>, and others<ref name="pmid17178826">{{cite journal |author=Cullen B, O'Neill B, Evans JJ, Coen RF, Lawlor BA |title=A review of screening tests for cognitive impairment |journal=J. Neurol. Neurosurg. Psychiatr. |volume=78 |issue=8 |pages=790–9 |year=2007 |pmid=17178826 |doi=10.1136/jnnp.2006.095414}}</ref>, have summarized the diagnostic accuracy of screening tests.
Normally, symptoms must be present for at least six months to support a diagnosis. Cognitive dysfunction of shorter duration is called delirium. Delirium can be easily confused with dementia due to similar symptoms. Delirium is characterized by a sudden onset, fluctuating course, a short duration (often lasting from hours to weeks), and is primarily related to a somatic (or medical) disturbance. In comparison, dementia has typically a long, slow onset (except in the cases of a stroke or trauma), slow decline of mental functioning, as well as a longer trajectory (from months to years).


The single best finding may be disoriented to year.<ref name="pmid20852313">{{cite journal| author=O'Keeffe E, Mukhtar O, O'Keeffe ST| title=Orientation to time as a guide to the presence and severity of cognitive impairment in older hospital patients. | journal=J Neurol Neurosurg Psychiatry | year= 2011 | volume= 82 | issue= 5 | pages= 500-4 | pmid=20852313 | doi=10.1136/jnnp.2010.214817 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20852313  }} </ref>
===Four functional symptoms===
Diagnosis of dementia is usually based on medical history and cognitive testing with imaging. Blood tests may be taken to rule out other possible causes that may be reversible, such as hypothyroidism, and to determine the dementia subtype. One commonly used cognitive test is the mini–mental state examination. Although the greatest risk factor for developing dementia is aging, dementia is not a normal part of the aging process; many people aged 90 and above show no signs of dementia. Several risk factors for dementia, such as smoking and obesity, are preventable by lifestyle changes.  


===Ascertainment of decision making capacity===
Deficits in cognitive function contribute to impaired functional status.<ref name="pmid17827410">{{cite journal |author=Royall DR, Lauterbach EC, Kaufer D, Malloy P, Coburn KL, Black KJ |title=The cognitive correlates of functional status: a review from the Committee on Research of the American Neuropsychiatric Association |journal=The Journal of neuropsychiatry and clinical neurosciences |volume=19 |issue=3 |pages=249–65 |year=2007 |pmid=17827410 |doi=10.1176/appi.neuropsych.19.3.249}}</ref> The deficits in the domains of cognitive function are<ref name="pmid17551132">{{cite journal |author=Holsinger T, Deveau J, Boustani M, Williams JW |title=Does this patient have dementia? |journal=JAMA |volume=297 |issue=21 |pages=2391–404 |year=2007 |pmid=17551132 |doi=10.1001/jama.297.21.2391}}</ref>:
* Agnosia - "Failure to recognize or identify objects despite intact sensory function"<ref name="pmid17551132"/>
* Aphasia - "Deterioration of language function"<ref name="pmid17551132"/>
* Apraxia - "Impaired ability to execute motor activities despite intact motor abilities, sensory function, and comprehension of the required task"<ref name="pmid17551132"/>
* Disturbance in executive functioning - "The ability to think abstractly and to plan, initiate, sequence, monitor, and stop complex behavior"<ref name="pmid17551132"/>
===Ascertainment of decision-making capacity===
Decision making can be assessed with the  [http://crashingpatient.com/wp-content/pdf/ACE.pdf Aid to Capacity  Evaluation] (ACE).<ref name="pmid21791691">{{cite journal|  author=Sessums LL, Zembrzuska H, Jackson JL| title=Does this patient  have medical decision-making capacity? | journal=JAMA | year= 2011 |  volume= 306 | issue= 4 | pages= 420-7 | pmid=21791691 |  doi=10.1001/jama.2011.1023 | pmc= |  url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21791691  }} </ref>
Decision making can be assessed with the  [http://crashingpatient.com/wp-content/pdf/ACE.pdf Aid to Capacity  Evaluation] (ACE).<ref name="pmid21791691">{{cite journal|  author=Sessums LL, Zembrzuska H, Jackson JL| title=Does this patient  have medical decision-making capacity? | journal=JAMA | year= 2011 |  volume= 306 | issue= 4 | pages= 420-7 | pmid=21791691 |  doi=10.1001/jama.2011.1023 | pmc= |  url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21791691  }} </ref>


===Consequences of labeling===
===Consequences of labeling===
In one study, learning of having ''mild'' cognitive impairment reduced stress.<ref> Carpenter, B. D., Xiong, C., Porensky, E. K., Lee, M. M., Brown, P. J., Coats, M., et al. (2008). Reaction to a dementia diagnosis in individuals with alzheimer's disease and mild cognitive impairment, Journal of the American Geriatrics Society, 56(3), 405-412. {{doi| doi:10.1111/j.1532-5415.2007.01600.x.}}</ref>
In one study, learning of having ''mild'' cognitive impairment reduced stress.<ref> Carpenter, B. D., Xiong, C., Porensky, E. K., Lee, M. M., Brown, P. J., Coats, M., et al. (2008). Reaction to a dementia diagnosis in individuals with Alzheimer's disease and mild cognitive impairment, Journal of the American Geriatrics Society, 56(3), 405-412. {{doi| doi:10.1111/j.1532-5415.2007.01600.x.}}</ref>
 
===Mental status schedules===
[[Systematic review]]s have compared the schedules.<ref name="pmid24145578">{{cite journal| author=Lin JS, O'Connor E, Rossom RC, Perdue LA, Eckstrom E| title=Screening for cognitive impairment in older adults: A systematic review for the U.S. Preventive Services Task Force. | journal=Ann Intern Med | year= 2013 | volume= 159 | issue= 9 | pages= 601-12 | pmid=24145578 | doi=10.7326/0003-4819-159-9-201311050-00730 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24145578  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24534934 Review in: Ann Intern Med. 2014 Feb 18;160(4):JC12] </ref><ref name="pmid17551132"/>


===Investigation of causes===
A separate [[systematic review]] has examined decision making capacity.<ref name="pmid21791691"/>
Among rapidly progressive cases, causes include:<ref name="pmid21674591">{{cite journal| author=Chitravas N, Jung RS, Kofskey DM, Blevins JE, Gambetti P, Leigh RJ et al.| title=Treatable neurological disorders misdiagnosed as Creutzfeldt-Jakob disease. | journal=Ann Neurol | year= 2011 | volume=  | issue=  | pages=  | pmid=21674591 | doi=10.1002/ana.22454 | pmc= | url= }}</ref>
* Sporadic Creutzfeldt-Jakob disease (sCJD)
* Immunological (vasculitis, encephalomyelitis, and limbic encephalitis)
* Neoplastic (mainly lymphoma)
* Infectious (fungal, viral, and parasitic)
* Metabolic (including [[Wernicke encephalopathy]])


==Temporal disorientation==
====Temporal disorientation====
Among hospitalized [[geriatrics|geriatric]] patients, "failure to identify either year or month correctly was 95% sensitive and  86.5% specific for the detection of cognitive impairment".<ref name="pmid20852313">{{cite journal| author=O'Keeffe E, Mukhtar O, O'Keeffe ST| title=Orientation to time as a guide to the presence and severity of cognitive impairment in older hospital patients. | journal=J Neurol Neurosurg Psychiatry | year= 2011 | volume= 82 | issue= 5 | pages= 500-4 | pmid=20852313 | doi=10.1136/jnnp.2010.214817 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20852313  }} </ref>
Among hospitalized [[geriatrics|geriatric]] patients, "failure to identify either year or month correctly was 95% sensitive and  86.5% specific for the detection of cognitive impairment".<ref name="pmid20852313">{{cite journal| author=O'Keeffe E, Mukhtar O, O'Keeffe ST| title=Orientation to time as a guide to the presence and severity of cognitive impairment in older hospital patients. | journal=J Neurol Neurosurg Psychiatry | year= 2011 | volume= 82 | issue= 5 | pages= 500-4 | pmid=20852313 | doi=10.1136/jnnp.2010.214817 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20852313  }} </ref>
Diagnostic surveys have been compared.<ref name="pmid22646750">{{cite journal| author=Holsinger T, Plassman BL, Stechuchak KM, Burke JR, Coffman CJ, Williams JW| title=Screening for cognitive impairment: comparing the performance of four instruments in primary care. | journal=J Am Geriatr Soc | year= 2012 | volume= 60 | issue= 6 | pages= 1027-36 | pmid=22646750 | doi=10.1111/j.1532-5415.2012.03967.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22646750  }} </ref>


====Sweet 16====
====Sweet 16====
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* [[sensitivity (tests)|sensitivity]] 99%
* [[sensitivity (tests)|sensitivity]] 99%
* [[specificity (tests)|specificity]] 72%
* [[specificity (tests)|specificity]] 72%
====Mini-cog====
According to the systematic review by the [http://jama.jamanetwork.com/collection.aspx?categoryid=6257 Rational Clinical Examination], regarding the mini-cog "the performance of the Mini-Cog...cannot be determined with confidence because none of these screens were actually administered in their suggested forms. However, the performance suggested by the retrospective analyses reported in these articles is promising."<ref name="pmid17551132">{{cite journal |author=Holsinger T, Deveau J, Boustani M, Williams JW |title=Does this patient have dementia? |journal=JAMA |volume=297 |issue=21 |pages=2391–404 |year=2007 |pmid=17551132 |doi=10.1001/jama.297.21.2391}}</ref> More recent studies<ref name="pmid23070510">{{cite journal| author=Hirsch C| title=The Mini-Cog had sensitivity similar to the longer 3MS for detecting cognitive impairment or dementia. | journal=Ann Intern Med | year= 2012 | volume= 157 | issue= 8 | pages= JC4-8 | pmid=23070510 | doi=10.7326/0003-4819-157-8-201210160-02008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23070510  }} </ref> and reviews<ref name="pmid20808118">{{cite journal| author=Mitchell AJ, Malladi S| title=Screening and case finding tools for the detection of dementia. Part I: evidence-based meta-analysis of multidomain tests. | journal=Am J Geriatr Psychiatry | year= 2010 | volume= 18 | issue= 9 | pages= 759-82 | pmid=20808118 | doi=10.1097/JGP.0b013e3181cdecb8 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20808118  }} </ref> are favorable. The mini-COG is available at http://www.hospitalmedicine.org/geriresource/toolbox/pdfs/clock_drawing_test.pdf and http://geriatrics.uthscsa.edu/tools/MINICog.pdf .


====Mini-mental state examination====
====Mini-mental state examination====
The Mini-mental state examination (MMSE) is the most studied test.<ref name="pmid17551132"/> A [[systematic review]] concluded that the accuracy of the MMSE is:<ref name="pmid12779304"/>:
The Mini-mental state examination (MMSE) is the most studied test. A [[systematic review]] concluded that the accuracy of the MMSE is:
* [[sensitivity (tests)|sensitivity]] 71% to 92%
* [[sensitivity (tests)|sensitivity]] 71% to 92%
* [[specificity (tests)|specificity]] 56% to 96%
* [[specificity (tests)|specificity]] 56% to 96%


Copies of ther MMSE can be purchased (http://www4.parinc.com/Products/Product.aspx?ProductID=MMSE). A copy of the Mini-mental state examination can be found in the appendix of the original publication.<ref name="pmid1202204">{{cite journal |author=Folstein MF, Folstein SE, McHugh PR |title="Mini-mental state". A practical method for grading the cognitive state of patients for the clinician |journal=Journal of psychiatric research |volume=12 |issue=3 |pages=189-98 |year=1975 |pmid=1202204 |doi=10.1016/0022-3956(75)90026-6}}</ref>
Copies of their MMSE can be purchased (http://www4.parinc.com/Products/Product.aspx?ProductID=MMSE). A copy of the Mini-mental state examination can be found in the appendix of the original publication.<ref name="pmid1202204">{{cite journal |author=Folstein MF, Folstein SE, McHugh PR |title="Mini-mental state". A practical method for grading the cognitive state of patients for the clinician |journal=Journal of psychiatric research |volume=12 |issue=3 |pages=189-98 |year=1975 |pmid=1202204 |doi=10.1016/0022-3956(75)90026-6}}</ref>


====Modified Mini-Mental State examination (3MS)====
====Modified Mini-Mental State examination (3MS)====
A [[meta-analysis]] concluded that the Modified Mini-Mental State (3MS) examination has:<ref name="pmid17178826"/>
A [[meta-analysis]] concluded that the Modified Mini-Mental State (3MS) examination has:
* [[sensitivity (tests)|sensitivity]] 83% to 94%
* [[sensitivity (tests)|sensitivity]] 83% to 94%
* [[specificity (tests)|specificity]] 85% to 90%
* [[specificity (tests)|specificity]] 85% to 90%
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====Abbreviated mental test score====
====Abbreviated mental test score====
A [[meta-analysis]] concluded:<ref name="pmid17178826"/>
A [[meta-analysis]] concluded:
: [[sensitivity (tests)|sensitivity]] 73% to 100%
: [[sensitivity (tests)|sensitivity]] 73% to 100%
: [[specificity (tests)|specificity]] 71% to 100%
: [[specificity (tests)|specificity]] 71% to 100%
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| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=8232972 }} </ref>
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=8232972 }} </ref>


====Clock drawing task====
{| class="wikitable" align="center"
|-
! Dementia type
! CLOX1<br>(Executive control)
! CLOX2<br>(Posterior cortical)
! Pentagons copying<br>on MMSE
!Total MMSE score
|-
| Posterior cortical and<br>diffuse cortical<br>dementias
| Abnormal
| Abnormal
| Abnormal
| Abnormal
|-
| Subcortical and<br>frontal cortical<br>dementias
| ''Abnormal''
| Normal
| Normal
| Normal
|}


The Clock drawing task (CLOX) consists of two tests and is available online at PubMed Central.<ref name="pmid9598672">{{cite journal |author=Royall, D.; Cordes J.; & Polk M. |title=CLOX: an executive clock drawing task |journal=J Neurol Neurosurg Psychiatry |volume=64 |issue=5 |pages=588-94 |year=1998 |pmid=9598672 | url=http://jnnp.bmj.com/cgi/content/full/64/5/588}} [http://www.pubmedcentral.nih.gov/articlerender.fcgi?pubmedid=9598672 Full text at PubMed Central]  [http://jnnp.bmj.com/cgi/content/full/64/5/588/F3 Example form]</ref> The CLOX1 task has the subject draw a clock face without any prompting other than the instructions "Draw me a clock that says 1:45. Set the hands and numbers on the face so that a child could read them". The CLOX1 is tests executive function and correlates with the EXIT25 test of executive function. The CLOX2 task has the subject copy a clock face from an example, does not test executive function and correlates with the MMSE.
====St Louis University mental status examination (SLUMS)====
The SLUMS has been compared to the MMSE.<ref name="pmid24916485">{{cite journal| author=Cummings-Vaughn LA, Chavakula NN, Malmstrom TK, Tumosa N, Morley JE, Cruz-Oliver DM| title=Veterans affairs saint louis university mental status examination compared with the montreal cognitive assessment and the short test of mental status. | journal=J Am Geriatr Soc | year= 2014 | volume= 62 | issue= 7 | pages= 1341-6 | pmid=24916485 | doi=10.1111/jgs.12874 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24916485  }} </ref><ref name="pmid17068312">{{cite journal| author=Tariq SH, Tumosa N, Chibnall JT, Perry MH, Morley JE| title=Comparison of the Saint Louis University mental status examination and the mini-mental state examination for detecting dementia and mild neurocognitive disorder--a pilot study. | journal=Am J Geriatr Psychiatry | year= 2006 | volume= 14 | issue= 11 | pages= 900-10 | pmid=17068312 | doi=10.1097/01.JGP.0000221510.33817.86 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17068312  }} </ref> Both evaluations were by the developer of the SLUMS and showed comparable accuracy to the MMSE.


The CLOX may avoid the bias of the MMSE toward cortical dementias.<ref name="pmid9598672"/> In addition, "as Alzheimer’s disease affects posterior cortical regions before invading the frontal cortex, isolated ECF impairment (CLOX1) is not likely to represent early Alzheimer’s disease."<ref name="pmid9598672"/> Thus, isolated abnormalities of the CLOX1 may be able to detect reversible dementias such as subcortical [[stroke]], [[depression]], [[vitamin B12 deficiency]], [[polypharmacy]], and [[hypothyroidism]].<ref name="pmid9598672"/>
====Other examinations====
Many other tests have been studied <ref name="pmid17163083">{{cite journal |author=Sager, M.; Hermann, B.; La Rue, A.; & Woodard, J. |title=Screening for dementia in community-based memory clinics |journal=WMJ |volume=105 |issue=7 |pages=25-9 |year=2006 |pmid=17163083}}</ref><ref name="pmid17287448">{{cite journal |author=Fleisher, A.; Sowell B.; Taylor C.; Gamst A.; Petersen R.; & Thal L. |title=Clinical predictors of progression to Alzheimer's disease in amnestic mild cognitive impairment |journal=Neurology |volume=68 |issue=19 |pages=1588-95 |year=2007 |pmid=17287448}}</ref><ref name="pmid12614094">[https://doi.org/10.7326/0003-4819-138-5-200303040-00011 Diagnostic evaluation of elderly patients with mild memory problems] by Jason H T Karlawish and Christopher M Clark,    PMID 12614094 DOI 10.7326/0003-4819-138-5-200303040-00011</ref> including the Executive Interview (EXIT)<ref>Royall DR, Mahurin RK, Gray KF. Bedside assessment of executive cognitive impairment: the executive interview. J Am Geriatr Soc. 1992;40:1221-6. PMID 1447438</ref>.<ref name="pmid21496140">{{cite journal| author=Carpenter CR, Bassett ER, Fischer GM, Shirshekan J, Galvin JE, Morris JC| title=Four sensitive screening tools to detect cognitive dysfunction in geriatric emergency department patients: brief Alzheimer's Screen, Short Blessed Test, Ottawa 3DY, and the caregiver-completed AD8. | journal=Acad Emerg Med | year= 2011 | volume= 18 | issue= 4 | pages= 374-84 | pmid=21496140 | doi=10.1111/j.1553-2712.2011.01040.x | pmc=PMC3080244 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21496140  }} </ref>


====Other examinations====
===Investigation of causes===
Many other tests have been studied <ref name="pmid17163083">{{cite journal |author=Sager, M.; Hermann, B.; La Rue, A.; & Woodard, J. |title=Screening for dementia in community-based memory clinics |journal=WMJ |volume=105 |issue=7 |pages=25-9 |year=2006 |pmid=17163083}}</ref><ref name="pmid17287448">{{cite journal |author=Fleisher, A.; Sowell B.; Taylor C.; Gamst A.; Petersen R.; & Thal L. |title=Clinical predictors of progression to Alzheimer disease in amnestic mild cognitive impairment |journal=Neurology |volume=68 |issue=19 |pages=1588-95 |year=2007 |pmid=17287448}}</ref><ref name="pmid12614094"/> including the Executive Interview (EXIT)<ref>Royall DR, Mahurin RK, Gray KF. Bedside assessment of executive cognitive impairment: the executive interview. J Am Geriatr Soc. 1992;40:1221-6. PMID 1447438</ref>.
Among rapidly progressive cases, causes include:<ref name="pmid21674591">{{cite journal| author=Chitravas N, Jung RS, Kofskey DM, Blevins JE, Gambetti P, Leigh RJ et al.| title=Treatable neurological disorders misdiagnosed as Creutzfeldt-Jakob disease. | journal=Ann Neurol | year= 2011 | volume= | issue= | pages= | pmid=21674591 | doi=10.1002/ana.22454 | pmc= | url= }}</ref>
sporadic, e.g., Creutzfeldt-Jakob disease (sCJD), immunological (vasculitis, encephalomyelitis, and limbic encephalitis), cancer (mainly lymphoma), infectious (fungal, viral, and parasitic), and metabolic (including [[Wernicke encephalopathy]]) causes.


===Laboratory tests===
===Laboratory tests===
====Apolipoprotein E4====
====Apolipoprotein E4====
Although [[apolipoprotein E4]] is an important susceptibility gene for [[Alzheimer's disease]]<ref name="pmid10944568">{{cite journal |author=Skoog I |title=Detection of preclinical Alzheimer's disease |journal=N. Engl. J. Med. |volume=343 |issue=7 |pages=502–3 |year=2000 |month=August |pmid=10944568 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=10944568&promo=ONFLNS19 |issn= |quote=The APOE 4 allele is a susceptibility gene for Alzheimer's disease and seems to affect the age of onset of the disease. However, the presence of this allele alone is not sufficient to predict which asymptomatic subjects will ultimately have Alzheimer's disease, and the disease never develops in many subjects with this genotype}}</ref>, its [[sensitivity and specificity]] are insufficient (65 and 68 percent, respectively) to be used as a diagnostic test.<ref name="pmid12160362">{{cite journal |author=Kivipelto M, Helkala EL, Laakso MP, ''et al'' |title=Apolipoprotein E epsilon4 allele, elevated midlife total cholesterol level, and high midlife systolic blood pressure are independent risk factors for late-life Alzheimer disease |journal=Ann. Intern. Med. |volume=137 |issue=3 |pages=149–55 |year=2002 |month=August |pmid=12160362 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=reprint&pmid=12160362 |issn=}}</ref>
Although [[apolipoprotein E4]] is an important susceptibility gene for [[Alzheimer's disease]]<ref name="pmid10944568">{{cite journal |author=Skoog I |title=Detection of preclinical Alzheimer's disease |journal=N. Engl. J. Med. |volume=343 |issue=7 |pages=502–3 |year=2000 |month=August |pmid=10944568 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=10944568&promo=ONFLNS19 |issn= |quote=The APOE 4 allele is a susceptibility gene for Alzheimer's disease and seems to affect the age of onset of the disease. However, the presence of this allele alone is not sufficient to predict which asymptomatic subjects will ultimately have Alzheimer's disease, and the disease never develops in many subjects with this genotype}}</ref>, its [[sensitivity and specificity]] are insufficient (65 and 68 percent, respectively) to be used as a diagnostic test.<ref name="pmid12160362">{{cite journal |author=Kivipelto M, Helkala EL, Laakso MP, ''et al'' |title=Apolipoprotein E epsilon4 allele, elevated midlife total cholesterol level, and high midlife systolic blood pressure are independent risk factors for late-life Alzheimer's disease |journal=Ann. Intern. Med. |volume=137 |issue=3 |pages=149–55 |year=2002 |month=August |pmid=12160362 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=reprint&pmid=12160362 |issn=}}</ref>


[[Apolipoprotein E4]] does not added to other tests in predicting who will develop Alzheimer's.<ref name="pmid18723162">{{cite journal |author=Devanand DP, Liu X, Tabert MH, ''et al'' |title=Combining early markers strongly predicts conversion from mild cognitive impairment to Alzheimer's disease |journal=Biol. Psychiatry |volume=64 |issue=10 |pages=871–9 |year=2008 |month=November |pmid=18723162 |doi=10.1016/j.biopsych.2008.06.020 |url=http://linkinghub.elsevier.com/retrieve/pii/S0006-3223(08)00788-9 |issn=}}</ref>
[[Apolipoprotein E4]] does not added to other tests in predicting who will develop Alzheimer's.<ref name="pmid18723162">{{cite journal |author=Devanand DP, Liu X, Tabert MH, ''et al'' |title=Combining early markers strongly predicts conversion from mild cognitive impairment to Alzheimer's disease |journal=Biol. Psychiatry |volume=64 |issue=10 |pages=871–9 |year=2008 |month=November |pmid=18723162 |doi=10.1016/j.biopsych.2008.06.020 |url=http://linkinghub.elsevier.com/retrieve/pii/S0006-3223(08)00788-9 |issn=}}</ref>
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Home-based program of physical activity might benefit according to a [[randomized controlled trial]].<ref>Lautenschlager NT, Cox KL, Flicker L, Foster JK, van Bockxmeer FM, Xiao J, et al. [http://jama.ama-assn.org/cgi/content/full/300/9/1027 Effect of Physical Activity on Cognitive Function in Older Adults at Risk for Alzheimer Disease: A Randomized Trial]. JAMA. 2008 Sep 3;300(9):1027-1037.</ref>
Home-based program of physical activity might benefit according to a [[randomized controlled trial]].<ref>Lautenschlager NT, Cox KL, Flicker L, Foster JK, van Bockxmeer FM, Xiao J, et al. [http://jama.ama-assn.org/cgi/content/full/300/9/1027 Effect of Physical Activity on Cognitive Function in Older Adults at Risk for Alzheimer Disease: A Randomized Trial]. JAMA. 2008 Sep 3;300(9):1027-1037.</ref>


====Bright lights====
Any initial randomized controlled trial suggests that bright light helps.<ref name="pmid18544724">{{cite journal |author=Riemersma-van der Lek RF, Swaab DF, Twisk J, Hol EM, Hoogendijk WJ, Van Someren EJ |title=Effect of bright light and melatonin on cognitive and noncognitive function in elderly residents of group care facilities: a randomized controlled trial |journal=JAMA |volume=299 |issue=22 |pages=2642–55 |year=2008 |month=June |pmid=18544724 |doi=10.1001/jama.299.22.2642 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18544724 |issn=}}</ref>


===Medications===
===Medications===
According to the [[clinical practice guideline]] by the [[American College of Physicians]], "the evidence is insufficient to compare the effectiveness of different pharmacologic agents for the treatment of dementia."<ref name="pmid18316755">{{cite journal |author=Qaseem A, Snow V, Cross JT, ''et al'' |title=Current pharmacologic treatment of dementia: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians |journal=Ann. Intern. Med. |volume=148 |issue=5 |pages=370–8 |year=2008 |month=March |pmid=18316755 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=18316755 |issn=}}</ref>
As of 2024, especially regarding Alzheimer's, there are generally no effective medications to either reverse or halt dementia progression. This includes new drugs such as the Alzheimer's anti-beta amyloid monoclonal antibody drug leqembi, which slightly slows the progression of Alzheimer's but does not stop it.
 
"Treatment of dementia with cholinesterase inhibitors and memantine can result in statistically significant but clinically marginal improvement in measures of cognition and global assessment of dementia" according to a [[systematic review]] for the [[clinical practice guideline]].<ref name="pmid18316756">{{cite journal |author=Raina P, Santaguida P, Ismaila A, ''et al'' |title=Effectiveness of cholinesterase inhibitors and memantine for treating dementia: evidence review for a clinical practice guideline |journal=Ann. Intern. Med. |volume=148 |issue=5 |pages=379–97 |year=2008 |month=March |pmid=18316756 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=18316756 |issn=}}</ref>


====Cholinesterase inhibitors====
Cholinesterase inhibitors.
Available cholinesterase inhibitors drugs are donepezil, galantamine, rivastigmine, and tacrine.
Available cholinesterase inhibitors drugs are donepezil, galantamine, rivastigmine, and tacrine.


====Neuropeptide-modifier====
Neuropeptide modifier.
Memantine is a neuropeptide-modifier that acts on the N-Methyl-D-Aspartate (NMDA) [[cell surface receptor]]s for the [[neurotransmitter]] [[glutamate]].
Memantine is a neuropeptide modifier that acts on the N-methyl-D-aspartate (NMDA) [[cell surface receptor]]s for the [[neurotransmitter]] [[glutamate]].


====Anti-psychotics====
Anti-psychotics.
The newer, atypical [[antipsychotic agent]]s (olanzapine, quetiapine, risperidone), were found to have "adverse effects offset advantages in the efficacy of atypical antipsychotic drugs for the treatment of psychosis, aggression, or agitation in patients with Alzheimer's disease."<ref name="pmid17035647">{{cite journal |author=Schneider LS, Tariot PN, Dagerman KS, ''et al'' |title=Effectiveness of atypical antipsychotic drugs in patients with Alzheimer's disease |journal=N. Engl. J. Med. |volume=355 |issue=15 |pages=1525–38 |year=2006 |pmid=17035647 |doi=10.1056/NEJMoa061240|url=http://content.nejm.org/cgi/content/full/355/15/1525}}</ref> A more recent [[randomized controlled trial]] that compared the second generation anti-psychotic agents found that none improved functioning, care needs, or quality of life with [[statistical significance]]<ref name="pmid17035647">{{cite journal| author=Schneider LS, Tariot PN, Dagerman KS, Davis SM, Hsiao JK, Ismail MS et al.| title=Effectiveness of atypical antipsychotic drugs in patients with Alzheimer's disease. | journal=N Engl J Med | year= 2006 | volume= 355 | issue= 15 | pages= 1525-38 | pmid=17035647
The newer, atypical [[antipsychotic agent]]s (olanzapine, quetiapine, risperidone), were found to have "adverse effects offset advantages in the efficacy of atypical antipsychotic drugs for the treatment of psychosis, aggression, or agitation in patients with Alzheimer's disease."<ref name="pmid17035647">{{cite journal |author=Schneider LS, Tariot PN, Dagerman KS, ''et al'' |title=Effectiveness of atypical antipsychotic drugs in patients with Alzheimer's disease |journal=N. Engl. J. Med. |volume=355 |issue=15 |pages=1525–38 |year=2006 |pmid=17035647 |doi=10.1056/NEJMoa061240|url=http://content.nejm.org/cgi/content/full/355/15/1525}}</ref> A more recent [[randomized controlled trial]] that compared the second generation anti-psychotic agents found that none improved functioning, care needs, or quality of life with [[statistical significance]]<ref name="pmid17035647"/>; however, olanzapine and risperidone may reduce anger.<ref name="pmid18519523">{{cite journal| author=Sultzer DL, Davis SM, Tariot PN, Dagerman KS, Lebowitz BD, Lyketsos CG et al.| title=Clinical symptom responses to atypical antipsychotic medications in Alzheimer's disease: phase 1 outcomes from the CATIE-AD effectiveness trial. | journal=Am J Psychiatry | year= 2008 | volume= 165 | issue= 7 | pages= 844-54 | pmid=18519523  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=17035647 | doi=10.1056/NEJMoa061240 }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=17335158 Review in: ACP J Club. 2007 Mar-Apr;146(2):35]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=17459989 Review in: Evid Based Ment Health. 2007 May;10(2):58]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=17607819 Review in: J Fam Pract. 2007 Jan;56(1):14] </ref>; however, olanzapine and risperidone may reduce anger.<ref name="pmid18519523">{{cite journal| author=Sultzer DL, Davis SM, Tariot PN, Dagerman KS, Lebowitz BD, Lyketsos CG et al.| title=Clinical symptom responses to atypical antipsychotic medications in Alzheimer's disease: phase 1 outcomes from the CATIE-AD effectiveness trial. | journal=Am J Psychiatry | year= 2008 | volume= 165 | issue= 7 | pages= 844-54 | pmid=18519523  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=18519523 | doi=10.1176/appi.ajp.2008.07111779 | pmc=PMC2714365 }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19176779 Review in: Evid Based Ment Health. 2009 Feb;12(1):20] </ref> Regardless, [[antipsychotic agent]]s may increase mortality.<ref name="pmid19138567">{{cite journal| author=Ballard C, Hanney ML, Theodoulou M, Douglas S, McShane R, Kossakowski K et al.| title=The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial. | journal=Lancet Neurol | year= 2009 | volume= 8 | issue= 2 | pages= 151-7 | pmid=19138567  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=18519523 | doi=10.1176/appi.ajp.2008.07111779 | pmc=PMC2714365 }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19176779 Review in: Evid Based Ment Health. 2009 Feb;12(1):20] </ref> Regardless, [[antipsychotic agent]]s may increase mortality.<ref name="pmid19138567">{{cite journal| author=Ballard C, Hanney ML, Theodoulou M, Douglas S, McShane R, Kossakowski K et al.| title=The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial. | journal=Lancet Neurol | year= 2009 | volume= 8 | issue= 2 | pages= 151-7 | pmid=19138567  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19138567 | doi=10.1016/S1474-4422(08)70295-3 }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19528553 Review in: Ann Intern Med. 2009 Jun 16;150(12):JC6-8]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19648431 Review in: Evid Based Med. 2009 Aug;14(4):115] </ref>
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19138567 | doi=10.1016/S1474-4422(08)70295-3 }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19528553 Review in: Ann Intern Med. 2009 Jun 16;150(12):JC6-8]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19648431 Review in: Evid Based Med. 2009 Aug;14(4):115] </ref>
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Withdrawing psychotropics agents may prevent [[accidental fall]]s.<ref name="pmid10404930">{{cite journal |author=Campbell AJ, Robertson MC, Gardner MM, Norton RN, Buchner DM |title=Psychotropic medication withdrawal and a home-based exercise program to prevent falls: a randomized, controlled trial |journal=J Am Geriatr Soc |volume=47 |issue=7 |pages=850–3 |year=1999 |pmid=10404930 |doi=}}</ref>
Withdrawing psychotropics agents may prevent [[accidental fall]]s.<ref name="pmid10404930">{{cite journal |author=Campbell AJ, Robertson MC, Gardner MM, Norton RN, Buchner DM |title=Psychotropic medication withdrawal and a home-based exercise program to prevent falls: a randomized, controlled trial |journal=J Am Geriatr Soc |volume=47 |issue=7 |pages=850–3 |year=1999 |pmid=10404930 |doi=}}</ref>


====Melatonin====
Melatonin.
[[Melatonin]] may<ref name="pmid18070004">{{cite journal| author=Dowling GA, Burr RL, Van Someren EJ, Hubbard EM, Luxenberg JS, Mastick J et al.| title=Melatonin and bright-light treatment for rest-activity disruption in institutionalized patients with Alzheimer's disease. | journal=J Am Geriatr Soc | year= 2008 | volume= 56 | issue= 2 | pages= 239-46 | pmid=18070004  
Melatonin may<ref name="pmid18070004">{{cite journal| author=Dowling GA, Burr RL, Van Someren EJ, Hubbard EM, Luxenberg JS, Mastick J et al.| title=Melatonin and bright-light treatment for rest-activity disruption in institutionalized patients with Alzheimer's disease. | journal=J Am Geriatr Soc | year= 2008 | volume= 56 | issue= 2 | pages= 239-46 | pmid=18070004  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=18070004 | doi=10.1111/j.1532-5415.2007.01543.x | pmc=PMC2642966 }} </ref>or may not<ref name="pmid19155748">{{cite journal| author=Gehrman PR, Connor DJ, Martin JL, Shochat T, Corey-Bloom J, Ancoli-Israel S| title=Melatonin fails to improve sleep or agitation in double-blind randomized placebo-controlled trial of institutionalized patients with Alzheimer disease. | journal=Am J Geriatr Psychiatry | year= 2009 | volume= 17 | issue= 2 | pages= 166-9 | pmid=19155748  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=18070004 | doi=10.1111/j.1532-5415.2007.01543.x | pmc=PMC2642966 }} </ref>or may not<ref name="pmid19155748">{{cite journal| author=Gehrman PR, Connor DJ, Martin JL, Shochat T, Corey-Bloom J, Ancoli-Israel S| title=Melatonin fails to improve sleep or agitation in double-blind randomized placebo-controlled trial of institutionalized patients with Alzheimer disease. | journal=Am J Geriatr Psychiatry | year= 2009 | volume= 17 | issue= 2 | pages= 166-9 | pmid=19155748  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19155748 | doi=10.1097/JGP.0b013e318187de18 | pmc=PMC2630117 }} </ref><ref name="pmid14655926">{{cite journal| author=Singer C, Tractenberg RE, Kaye J, Schafer K, Gamst A, Grundman M et al.| title=A multicenter, placebo-controlled trial of melatonin for sleep disturbance in Alzheimer's disease. | journal=Sleep | year= 2003 | volume= 26 | issue= 7 | pages= 893-901 | pmid=14655926  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19155748 | doi=10.1097/JGP.0b013e318187de18 | pmc=PMC2630117 }} </ref><ref name="pmid14655926">{{cite journal| author=Singer C, Tractenberg RE, Kaye J, Schafer K, Gamst A, Grundman M et al.| title=A multicenter, placebo-controlled trial of melatonin for sleep disturbance in Alzheimer's disease. | journal=Sleep | year= 2003 | volume= 26 | issue= 7 | pages= 893-901 | pmid=14655926  
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| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=11180494 }} </ref> help with associated sleep and behavior disturbance.
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=11180494 }} </ref> help with associated sleep and behavior disturbance.


====Dietary supplements====
Dietary supplements.
[[Ginkgo biloba]] has conflicting evidence regarding its efficacy.<ref name="pmid12186600">{{cite journal |author=Solomon PR, Adams F, Silver A, Zimmer J, DeVeaux R |title=Ginkgo for memory enhancement: a randomized controlled trial |journal=JAMA |volume=288 |issue=7 |pages=835–40 |year=2002 |pmid=12186600 |doi=}}</ref><ref name="pmid9343463">{{cite journal |author=Le Bars PL, Katz MM, Berman N, Itil TM, Freedman AM, Schatzberg AF |title=A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group |journal=JAMA |volume=278 |issue=16 |pages=1327–32 |year=1997 |pmid=9343463 |doi=}}</ref><ref name="pmid19160216">{{cite journal |author=Birks J, Grimley Evans J |title=Ginkgo biloba for cognitive impairment and dementia |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD003120 |year=2009 |pmid=19160216 |doi=10.1002/14651858.CD003120.pub3 |url=http://dx.doi.org/10.1002/14651858.CD003120.pub3 |issn=}}</ref>
[[Ginkgo biloba]] has conflicting evidence regarding its efficacy.<ref name="pmid12186600">{{cite journal |author=Solomon PR, Adams F, Silver A, Zimmer J, DeVeaux R |title=Ginkgo for memory enhancement: a randomized controlled trial |journal=JAMA |volume=288 |issue=7 |pages=835–40 |year=2002 |pmid=12186600 |doi=}}</ref><ref name="pmid9343463">{{cite journal |author=Le Bars PL, Katz MM, Berman N, Itil TM, Freedman AM, Schatzberg AF |title=A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group |journal=JAMA |volume=278 |issue=16 |pages=1327–32 |year=1997 |pmid=9343463 |doi=}}</ref><ref name="pmid19160216">{{cite journal |author=Birks J, Grimley Evans J |title=Ginkgo biloba for cognitive impairment and dementia |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD003120 |year=2009 |pmid=19160216 |doi=10.1002/14651858.CD003120.pub3 |url=http://dx.doi.org/10.1002/14651858.CD003120.pub3 |issn=}}</ref>


{| class="wikitable"
Analgesics.
|+ [[Randomized controlled trial]]s of B vitamins<ref name="pmid20861451">{{cite journal| author=Ford AH, Flicker L, Alfonso H, Thomas J, Clarnette R, Martins R et al.| title=Vitamins B(12), B(6), and folic acid for cognition in older men. | journal=Neurology | year= 2010 | volume= 75 | issue= 17 | pages= 1540-7 | pmid=20861451 | doi=10.1212/WNL.0b013e3181f962c4 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20861451  }} </ref> <ref name="pmid18854539">{{cite journal| author=Aisen PS, Schneider LS, Sano M, Diaz-Arrastia R, van Dyck CH, Weiner MF et al.| title=High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial. | journal=JAMA | year= 2008 | volume= 300 | issue= 15 | pages= 1774-83 | pmid=18854539 | doi=10.1001/jama.300.15.1774 | pmc=PMC2684821 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18854539  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19633254 Review in: Evid Based Ment Health. 2009 Aug;12(3):86]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19238605 Review in: Ann Intern Med. 2009 Feb 17;150(4):JC2-7]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19321834 Review in: Evid Based Nurs. 2009 Apr;12(2):57] </ref> <ref name="pmid17240287">{{cite journal| author=Durga J, van Boxtel MP, Schouten EG, Kok FJ, Jolles J, Katan MB et al.| title=Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial. | journal=Lancet | year= 2007 | volume= 369 | issue= 9557 | pages= 208-16 | pmid=17240287 | doi=10.1016/S0140-6736(07)60109-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17240287  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17474680 Review in: ACP J Club. 2007 May-Jun;146(3):71]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17537891 Review in: Evid Based Med. 2007 Jun;12(3):83] </ref> <ref name="pmid16807413">{{cite journal| author=McMahon JA, Green TJ, Skeaff CM, Knight RG, Mann JI, Williams SM| title=A controlled trial of homocysteine lowering and cognitive performance. | journal=N Engl J Med | year= 2006 | volume= 354 | issue= 26 | pages= 2764-72 | pmid=16807413 | doi=10.1056/NEJMoa054025 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16807413  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17255396 Review in: Evid Based Ment Health. 2007 Feb;10(1):27] </ref>
! rowspan="2"|Trial!!rowspan="2"| Patients!!rowspan="2"| Intervention!!rowspan="2"|Comparison !!rowspan="2"|Outcome!!colspan="2"|Results!!rowspan="2"|Comment
|-<br/>
! Intervention!!Control
|-
| Ford<ref name="pmid20861451"/><br/>2010|| &bull;&nbsp;&ge; 75 years old, with [[hypertension]] but without dementia or depression<br/>&bull;&nbsp;No restrictions on folic acid, vitamin B12, and homocysteine levels||&bull;&nbsp;2 mg/d of folate<br/>&bull;&nbsp;25 mg/d of vitamin B6<br/>&bull;&nbsp;400 microg/d of vitamin B12||Placebo||Tests of cognition|| &nbsp;|| &nbsp;||negative study, but positive trend
|-
| Aisen<ref name="pmid18854539"/><br/>2008|| &bull;&nbsp;Mild to moderate Alzheimers disease<br/>&bull;&nbsp;Normal folic acid, vitamin B12, and homocysteine levels|| &bull;&nbsp;5 mg/d of folate<br/>&bull;&nbsp;25 mg/d of vitamin B6<br/>&bull;&nbsp;1 mg/d of vitamin B12||Placebo||Tests of cognition|| &nbsp;|| &nbsp;||negative study
|-
| Durga<ref name="pmid17240287"/><br/>2007|| 50-70 years old<br/>&bull;&nbsp;raised plasma homocysteine<br/>&bull;&nbsp;normal serum vitamin B12|| 800 microg/d folate||Placebo||Tests of cognition|| &nbsp;||&nbsp;|| A secondary publication of a study of folate originally for effect on carotid intimal thickness. In the current study, 3 of 6 measures of cognitive function improved. This publication contains an evidence table that summarizes prior studies.
|-
| McMahon<ref name="pmid16807413"/><br/>2006|| &ge; 65 years old<br/>&bull;&nbsp;raised plasma homocysteine||&bull;&nbsp;1000 microg/d  folate<br/>&bull;&nbsp;500 microg/d of Vitamin B12<br/>&bull;&nbsp;10 mg/d of vitamin B6||Placebo|| Tests of cognition|| &nbsp;|| &nbsp;||negative study
|}
 
====Analgesics====
Treating [[pain]] may reduce agitation.<ref name="pmid21765198">{{cite journal| author=Husebo BS, Ballard C, Sandvik R, Nilsen OB, Aarsland D| title=Efficacy of treating pain to reduce behavioural disturbances in residents of nursing homes with dementia: cluster randomised clinical trial. | journal=BMJ | year= 2011 | volume= 343 | issue=  | pages= d4065 | pmid=21765198 | doi=10.1136/bmj.d4065 | pmc= | url= }} </ref>
Treating [[pain]] may reduce agitation.<ref name="pmid21765198">{{cite journal| author=Husebo BS, Ballard C, Sandvik R, Nilsen OB, Aarsland D| title=Efficacy of treating pain to reduce behavioural disturbances in residents of nursing homes with dementia: cluster randomised clinical trial. | journal=BMJ | year= 2011 | volume= 343 | issue=  | pages= d4065 | pmid=21765198 | doi=10.1136/bmj.d4065 | pmc= | url= }} </ref>


==Prevention==
==Prevention==
===Physical activity===
Risk factors for dementia include high blood pressure, high levels of cholesterol, vision loss, hearing loss, smoking, obesity, depression, inactivity, diabetes, lower levels of education, and low social contact. Overindulgence in alcohol, lack of sleep, anemia, traumatic brain injury, and air pollution can also increase the chance of developing dementia. Many of these risk factors, including the lower level of education, smoking, physical inactivity and diabetes, are modifiable. Several of the group are known as vascular risk factors. Managing these risk factors can reduce the risk of dementia in individuals in their late midlife or older age. A reduction in a number of these risk factors, such as switching to a high-fiber, low-fat, plant-based diet or quitting cigarette smoking, can give a positive outcome. The decreased risk achieved by adopting a healthy lifestyle is seen even in those with a high genetic risk.
 
The standard American diet high in animal products and dairy and concomitant elevated levels of saturated fat is associated with a greater risk of developing dementia. Population and clinical research studies show that plant-based diets low in animal products and high in starch, fruits, and vegetables are associated with lower risk.
 
Most,<ref name="pmid8768414">{{cite journal |author=Byles JE, Sanson-Fisher RW |title=Mass mailing campaigns to promote screening for cervical cancer: do they work, and do they continue to work? |journal=Aust N Z J Public Health |volume=20 |issue=3 |pages=254–60 |year=1996 |month=June |pmid=8768414 |doi= |url= |issn=}}</ref><ref name="pmid18094335">{{cite journal |author=Ravaglia G, Forti P, Lucicesare A, ''et al'' |title=Physical activity and dementia risk in the elderly. Findings from a prospective Italian study |journal=Neurology |volume= |issue= |pages= |year=2007 |pmid=18094335 |doi=10.1212/01.wnl.0000296276.50595.86 |issn=}}</ref><ref name="pmid16418406">{{cite journal |author=Larson EB, Wang L, Bowen JD, ''et al'' |title=Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older |journal=Ann. Intern. Med. |volume=144 |issue=2 |pages=73–81 |year=2006 |pmid=16418406 |doi= |issn=}}</ref><ref name="pmid15383515">{{cite journal |author=Abbott RD, White LR, Ross GW, Masaki KH, Curb JD, Petrovitch H |title=Walking and dementia in physically capable elderly men |journal=JAMA |volume=292 |issue=12 |pages=1447–53 |year=2004 |pmid=15383515 |doi=10.1001/jama.292.12.1447 |issn=}}</ref> but not all<ref name="pmid12815136">{{cite journal |author=Verghese J, Lipton RB, Katz MJ, ''et al'' |title=Leisure activities and the risk of dementia in the elderly |journal=N. Engl. J. Med. |volume=348 |issue=25 |pages=2508–16 |year=2003 |pmid=12815136 |doi=10.1056/NEJMoa022252 |issn=}}</ref> studies find that physical activity is associated with reduced risk of dementia. These observational studies cannot prove cause and effect.
Most,<ref name="pmid8768414">{{cite journal |author=Byles JE, Sanson-Fisher RW |title=Mass mailing campaigns to promote screening for cervical cancer: do they work, and do they continue to work? |journal=Aust N Z J Public Health |volume=20 |issue=3 |pages=254–60 |year=1996 |month=June |pmid=8768414 |doi= |url= |issn=}}</ref><ref name="pmid18094335">{{cite journal |author=Ravaglia G, Forti P, Lucicesare A, ''et al'' |title=Physical activity and dementia risk in the elderly. Findings from a prospective Italian study |journal=Neurology |volume= |issue= |pages= |year=2007 |pmid=18094335 |doi=10.1212/01.wnl.0000296276.50595.86 |issn=}}</ref><ref name="pmid16418406">{{cite journal |author=Larson EB, Wang L, Bowen JD, ''et al'' |title=Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older |journal=Ann. Intern. Med. |volume=144 |issue=2 |pages=73–81 |year=2006 |pmid=16418406 |doi= |issn=}}</ref><ref name="pmid15383515">{{cite journal |author=Abbott RD, White LR, Ross GW, Masaki KH, Curb JD, Petrovitch H |title=Walking and dementia in physically capable elderly men |journal=JAMA |volume=292 |issue=12 |pages=1447–53 |year=2004 |pmid=15383515 |doi=10.1001/jama.292.12.1447 |issn=}}</ref> but not all<ref name="pmid12815136">{{cite journal |author=Verghese J, Lipton RB, Katz MJ, ''et al'' |title=Leisure activities and the risk of dementia in the elderly |journal=N. Engl. J. Med. |volume=348 |issue=25 |pages=2508–16 |year=2003 |pmid=12815136 |doi=10.1056/NEJMoa022252 |issn=}}</ref> studies find that physical activity is associated with reduced risk of dementia. These observational studies cannot prove cause and effect.
===Mental activity===
"Exergaming" may help.<ref name="pmid22261206">{{cite journal| author=Anderson-Hanley C, Arciero PJ, Brickman AM, Nimon JP, Okuma N, Westen SC et al.| title=Exergaming and older adult cognition: a cluster randomized clinical trial. | journal=Am J Prev Med | year= 2012 | volume= 42 | issue= 2 | pages= 109-19 | pmid=22261206 | doi=10.1016/j.amepre.2011.10.016 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22261206  }} </ref>


Maintaining activities such as cognitive games and reading, playing musical instruments, and physical activities are associated with reduced the risk of dementia in an observational study.<ref name="pmid12815136">{{cite journal |author=Verghese J, Lipton RB, Katz MJ, ''et al'' |title=Leisure activities and the risk of dementia in the elderly |journal=N. Engl. J. Med. |volume=348 |issue=25 |pages=2508–16 |year=2003 |pmid=12815136 |doi=10.1056/NEJMoa022252 |issn=}}</ref>
Maintaining activities such as cognitive games and reading, playing musical instruments, and physical activities are associated with reduced the risk of dementia in an observational study.<ref name="pmid12815136">{{cite journal |author=Verghese J, Lipton RB, Katz MJ, ''et al'' |title=Leisure activities and the risk of dementia in the elderly |journal=N. Engl. J. Med. |volume=348 |issue=25 |pages=2508–16 |year=2003 |pmid=12815136 |doi=10.1056/NEJMoa022252 |issn=}}</ref>


===Medications===
Various medications have been associated with progression or prevention ([[cholinesterase inhibitor]]s, [[N-methyl-D-aspartate receptor]] antagonists, [[renin-angiotensin system]] blockers, and [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s) of dementia.<ref name="pmid17012333">{{cite journal |author=Ellul J, Archer N, Foy CM, ''et al'' |title=The effects of commonly prescribed drugs in patients with Alzheimer's disease on the rate of deterioration |journal=J. Neurol. Neurosurg. Psychiatr. |volume=78 |issue=3 |pages=233–9 |year=2007 |month=March |pmid=17012333 |doi=10.1136/jnnp.2006.104034 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=17012333 |issn=}}</ref>
Various medications have been associated with progression or prevention ([[cholinesterase inhibitor]]s, [[N-methyl-D-aspartate receptor]] antagonists, [[renin-angiotensin system]] blockers, and [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s) of dementia.<ref name="pmid17012333">{{cite journal |author=Ellul J, Archer N, Foy CM, ''et al'' |title=The effects of commonly prescribed drugs in patients with Alzheimer's disease on the rate of deterioration |journal=J. Neurol. Neurosurg. Psychiatr. |volume=78 |issue=3 |pages=233–9 |year=2007 |month=March |pmid=17012333 |doi=10.1136/jnnp.2006.104034 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=17012333 |issn=}}</ref>


Observational, non-ramdomized [[cohort study|cohort studies]] suggest that [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s (statins) may<ref name="pmid18663180">{{cite journal |author=Cramer C, Haan MN, Galea S, Langa KM, Kalbfleisch JD |title=Use of statins and incidence of dementia and cognitive impairment without dementia in a cohort study |journal=Neurology |volume=71 |issue=5 |pages=344–50 |year=2008 |month=July |pmid=18663180 |doi=10.1212/01.wnl.0000319647.15752.7b |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=18663180 |issn=}}</ref><ref name="pmid18931004">{{cite journal |author=Haag MD, Hofman A, Koudstaal PJ, Stricker BH, Breteler MM |title=Statins are associated with a reduced risk of Alzheimer disease regardless of lipophilicity. The Rotterdam Study |journal=J. Neurol. Neurosurg. Psychiatr. |volume=80 |issue=1 |pages=13–7 |year=2009 |month=January |pmid=18931004 |doi=10.1136/jnnp.2008.150433 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=18931004 |issn=}}</ref> or may not<ref name="pmid15699299">{{cite journal |author=Zandi PP, Sparks DL, Khachaturian AS, ''et al'' |title=Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study |journal=Arch. Gen. Psychiatry |volume=62 |issue=2 |pages=217–24 |year=2005 |month=February |pmid=15699299 |doi=10.1001/archpsyc.62.2.217 |url=http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=15699299 |issn=}}</ref><ref name="pmid15534246">{{cite journal |author=Li G, Higdon R, Kukull WA, ''et al'' |title=Statin therapy and risk of dementia in the elderly: a community-based prospective cohort study |journal=Neurology |volume=63 |issue=9 |pages=1624–8 |year=2004 |month=November |pmid=15534246 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15534246 |issn=}}</ref> prevent dementia.
Observational, non-randomized [[cohort study|cohort studies]] suggest that [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s (statins) may<ref name="pmid18663180">{{cite journal |author=Cramer C, Haan MN, Galea S, Langa KM, Kalbfleisch JD |title=Use of statins and incidence of dementia and cognitive impairment without dementia in a cohort study |journal=Neurology |volume=71 |issue=5 |pages=344–50 |year=2008 |month=July |pmid=18663180 |doi=10.1212/01.wnl.0000319647.15752.7b |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=18663180 |issn=}}</ref><ref name="pmid18931004">{{cite journal |author=Haag MD, Hofman A, Koudstaal PJ, Stricker BH, Breteler MM |title=Statins are associated with a reduced risk of Alzheimer disease regardless of lipophilicity. The Rotterdam Study |journal=J. Neurol. Neurosurg. Psychiatr. |volume=80 |issue=1 |pages=13–7 |year=2009 |month=January |pmid=18931004 |doi=10.1136/jnnp.2008.150433 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=18931004 |issn=}}</ref> or may not<ref name="pmid15699299">{{cite journal |author=Zandi PP, Sparks DL, Khachaturian AS, ''et al'' |title=Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study |journal=Arch. Gen. Psychiatry |volume=62 |issue=2 |pages=217–24 |year=2005 |month=February |pmid=15699299 |doi=10.1001/archpsyc.62.2.217 |url=http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=15699299 |issn=}}</ref><ref name="pmid15534246">{{cite journal |author=Li G, Higdon R, Kukull WA, ''et al'' |title=Statin therapy and risk of dementia in the elderly: a community-based prospective cohort study |journal=Neurology |volume=63 |issue=9 |pages=1624–8 |year=2004 |month=November |pmid=15534246 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15534246 |issn=}}</ref> prevent dementia.


===Supplements===
[[Ginkgo biloba]] does not prevent dementia according to a large [[randomized controlled trial]]<ref name="pmid19017911">{{cite journal |author=DeKosky ST, Williamson JD, Fitzpatrick AL, ''et al'' |title=Ginkgo biloba for prevention of dementia: a randomized controlled trial |journal=JAMA |volume=300 |issue=19 |pages=2253–62 |year=2008 |month=November |pmid=19017911 |doi=10.1001/jama.2008.683 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=19017911 |issn=}}</ref> and [[systematic review]]<ref name="pmid19160216">{{cite journal |author=Birks J, Grimley Evans J |title=Ginkgo biloba for cognitive impairment and dementia |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD003120 |year=2009 |pmid=19160216 |doi=10.1002/14651858.CD003120.pub3 |url=http://dx.doi.org/10.1002/14651858.CD003120.pub3 |issn=}}</ref> by the [[Cochrane Collaboration]] in spite of earlier studies that were positive<ref name="pmid12404671">{{cite journal |author=Mix JA, Crews WD |title=A double-blind, placebo-controlled, randomized trial of Ginkgo biloba extract EGb 761 in a sample of cognitively intact older adults: neuropsychological findings |journal=Hum Psychopharmacol |volume=17 |issue=6 |pages=267–77 |year=2002 |month=August |pmid=12404671 |doi=10.1002/hup.412 |url=http://dx.doi.org/10.1002/hup.412 |issn=}}</ref>.
[[Ginkgo biloba]] does not prevent dementia according to a large [[randomized controlled trial]]<ref name="pmid19017911">{{cite journal |author=DeKosky ST, Williamson JD, Fitzpatrick AL, ''et al'' |title=Ginkgo biloba for prevention of dementia: a randomized controlled trial |journal=JAMA |volume=300 |issue=19 |pages=2253–62 |year=2008 |month=November |pmid=19017911 |doi=10.1001/jama.2008.683 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=19017911 |issn=}}</ref> and [[systematic review]]<ref name="pmid19160216">{{cite journal |author=Birks J, Grimley Evans J |title=Ginkgo biloba for cognitive impairment and dementia |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD003120 |year=2009 |pmid=19160216 |doi=10.1002/14651858.CD003120.pub3 |url=http://dx.doi.org/10.1002/14651858.CD003120.pub3 |issn=}}</ref> by the [[Cochrane Collaboration]] in spite of earlier studies that were positive<ref name="pmid12404671">{{cite journal |author=Mix JA, Crews WD |title=A double-blind, placebo-controlled, randomized trial of Ginkgo biloba extract EGb 761 in a sample of cognitively intact older adults: neuropsychological findings |journal=Hum Psychopharmacol |volume=17 |issue=6 |pages=267–77 |year=2002 |month=August |pmid=12404671 |doi=10.1002/hup.412 |url=http://dx.doi.org/10.1002/hup.412 |issn=}}</ref>.


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Similarly, mortality can be predicted by the ADEPT score.<ref name="pmid21045099">{{cite journal| author=Mitchell SL, Miller SC, Teno JM, Kiely DK, Davis RB, Shaffer ML| title=Prediction of 6-month survival of nursing home residents with advanced dementia using ADEPT vs hospice eligibility guidelines. | journal=JAMA | year= 2010 | volume= 304 | issue= 17 | pages= 1929-35 | pmid=21045099 | doi=10.1001/jama.2010.1572 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21045099  }} </ref>
Similarly, mortality can be predicted by the ADEPT score.<ref name="pmid21045099">{{cite journal| author=Mitchell SL, Miller SC, Teno JM, Kiely DK, Davis RB, Shaffer ML| title=Prediction of 6-month survival of nursing home residents with advanced dementia using ADEPT vs hospice eligibility guidelines. | journal=JAMA | year= 2010 | volume= 304 | issue= 17 | pages= 1929-35 | pmid=21045099 | doi=10.1001/jama.2010.1572 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21045099  }} </ref>
==Legal issues==
As of 2024, when improved healthcare means that many people are living longer, there is growing concern about dementia, not just in aging patients but as a result of other health challenges.  However, physicians often do not agree among themselves on how to detect and define it.  And a medical diagnosis of dementia can have serious legal consequences, resulting (just for example) in a patient losing the right to manage their own finances or make their own medical decisions.  Thus, in the U.S., physicians "recommend" that Medicare patients (age 65 and over) be given a cognitive test as part of their annual wellness exam, but they stopped short of requiring such a test.
==Attribution==
{{WPAttribution}}


==References==
==References==
<references/>
{{reflist|2}}[[Category:Suggestion Bot Tag]]

Latest revision as of 08:41, 1 November 2024

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This editable Main Article is under development and subject to a disclaimer.

Dementia is a syndrome associated with many neurodegenerative diseases, characterized by a general decline in cognitive abilities that affects a person's ability to perform everyday activities. Dementia may involve problems with memory, thinking, behavior, and motor control. Aside from memory impairment and a disruption in thought patterns, the most common symptoms of dementia include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than might be caused by the normal aging process. Dementia is currently the seventh leading cause of death worldwide and has 10 million new cases reported every year (approximately one every three seconds).

History

Until the end of the 19th century, dementia was a much broader clinical concept. It included mental illness and any type of psychosocial incapacity, including reversible conditions. Dementia at this time simply referred to anyone who had lost the ability to reason, and was applied equally to psychosis, "organic" diseases like syphilis that can destroy the brain, and to the dementia associated with old age, which was attributed to "hardening of the arteries".

In Roman times, philosopher Emperor Marcus Aurelius, who lived from 161 to 180 C.E., feared falling into a state of dementia more than he feared death. He wrote:

"...if we live longer, there is no guarantee that our mind will likewise retain that power to comprehend and study the world which contributes to our experience of things divine and human. If dementia sets in, there will be no failure of such faculties as breathing, feeding, imagination, desire: before these go, the earlier extinction is of one's proper use of oneself, one's accurate assessment of the gradations of duty, one's ability to analyse impressions, one's understanding of whether the time has come to leave this life - these and all other matters which wholly depend on trained calculation. So we must have a sense of urgency, not only for the ever closer approach of death, but also because our comprehension of the world and our ability to pay proper attention will fade before we do." --Meditations 3:1, Marcus Aurelius

Possible causes

Various diseases and injuries to the brain, such as stroke, can give rise to dementia. However, the most common cause is Alzheimer's disease, a neurodegenerative disorder. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), has re-described dementia as a mild or major neurocognitive disorder with varying degrees of severity and many causative subtypes. The International Classification of Diseases (ICD-11) also classifies dementia as a neurocognitive disorder (NCD) with many forms or subclasses. Dementia is listed as an acquired brain syndrome, marked by a decline in cognitive function, and is contrasted with neurodevelopmental disorders. It is also described as a spectrum of disorders with causative subtypes of dementia based on a known disorder, such as Parkinson's disease for Parkinson's disease dementia, Huntington's disease for Huntington's disease dementia, vascular disease for vascular dementia, HIV infection causing HIV dementia, frontotemporal lobar degeneration for frontotemporal dementia, Lewy body disease for dementia with Lewy bodies, and prion diseases.[1] Subtypes of neurodegenerative dementias may also be based on the underlying pathology of misfolded proteins, such as synucleinopathies and tauopathies. The coexistence of more than one type of dementia is known as mixed dementia.

Many neurocognitive disorders may be caused by another medical condition or disorder, including brain tumors and subdural hematoma, endocrine disorders such as hypothyroidism and hypoglycemia, nutritional deficiencies including of thiamine and niacin, infections, immune disorders, liver or kidney failure, metabolic disorders such as Kufs disease, some leukodystrophies, and neurological disorders such as epilepsy and multiple sclerosis. Some of the neurocognitive deficits may sometimes show improvement with treatment of the causative medical condition.

Decades of published scientific research strongly implicate long-term exposure to low levels of aluminum in the development of Alzheimer's disease. This dementia was completely unknown to medicine before the proliferation of aluminum throughout industrialized societies beginning in the late 19th century.

Signs and symptoms

The signs and symptoms of dementia are termed as the neuropsychiatric symptoms—also known as the behavioral and psychological symptoms—of dementia. The behavioral symptoms can include agitation, restlessness, inappropriate behavior, sexual disinhibition, and verbal or physical aggression. These symptoms may result from impairments in cognitive inhibition. The psychological symptoms can include depression, hallucinations (most often visual), delusions, apathy, and anxiety. The most commonly affected areas of brain function include memory, language, attention, problem solving, and visuospatial function affecting perception and orientation. The symptoms progress at a continuous rate over several stages, and they vary across the dementia subtypes. Most types of dementia are slowly progressive with some deterioration of the brain well established before signs of the disorder become apparent. There are often other conditions present, such as high blood pressure or diabetes, and there can sometimes be as many as four of these comorbidities.

Signs of dementia include getting lost in a familiar neighborhood, using unusual words to refer to familiar objects, forgetting the name of a close family member or friend, forgetting old memories, and being unable to complete tasks independently, such as paying bills or balancing a checkbook.

People with dementia are more likely to have problems with incontinence than those of a comparable age without dementia; they are three times more likely to have urinary incontinence and four times more likely to have fecal incontinence.

Stages

The course of dementia is often described in four stages – pre-dementia, early, middle, and late, that show a pattern of progressive cognitive and functional impairment. More detailed descriptions can be arrived at by the use of numeric scales. These scales include the Global Deterioration Scale for Assessment of Primary Degenerative Dementia (GDS or Reisberg Scale), the Functional Assessment Staging Test (FAST), and the Clinical Dementia Rating (CDR). Using the GDS, which more accurately identifies each stage of the disease progression, a more detailed course is described in seven stages – two of which are broken down further into five and six degrees. Stage 7(f) is the final stage.

Classification

Vascular dementia can affect both cortical and subcortial locations.

Cortical dementias

Among the many causes of cortical dementia, common causes are:

Subcortical dementias

Among the many causes of subcortical dementia, common causes are Parkinson's disease, vitamin B12 deficiency, and some vascular dementias.

Epidemiology

The number of cases of dementia worldwide in 2021 was estimated at 55 million, with close to 10 million new cases each year.[3] According to a report by the World Health Organization, "In 2021, Alzheimer’s disease and other forms of dementia ranked as the seventh leading cause of death, killing 1.8 million lives." By 2050, the number of people living with dementia is estimated to be over 150 million globally. Around 7% of people over the age of 65 have dementia, with slightly higher rates (up to 10% of those over 65) in places with relatively high life expectancy. In the United States, an estimated 40% of those over the age of 85 years old will eventually develop Alzheimer's dementia. The prevalence of dementia differs in different world regions, ranging from 4.7% in Central Europe to 8.7% in North Africa/Middle East; the prevalence in other regions is estimated to be between 5.6 and 7.6%. The number of people living with dementia is estimated to double every 20 years. In 2016 dementia resulted in about 2.4 million deaths, up from 0.8 million in 1990.

The annual incidence of dementia diagnosis is nearly 10 million worldwide. Almost half of new dementia cases occur in Asia, followed by Europe (25%), the Americas (18%), and Africa (8%). The incidence of dementia increases exponentially with age, doubling with every 6.3-year increase in age.[4] Rates are slightly higher in women than men at ages 65 and greater. The disease trajectory is varied and the median time from diagnosis to death depends strongly on age at diagnosis, from 6.7 years for people diagnosed aged 60–69 to 1.9 years for people diagnosed at 90 or older.

Dementia impacts not only individuals with dementia, but also their carers and the wider society. Among people aged 60 years and over, dementia is ranked the ninth most burdensome condition according to the 2010 Global Burden of Disease (GBD) estimates. The global costs of dementia was around U.S. $818 billion in 2015, a 35.4% increase from U.S. $604 billion in 2010.

A new 2024 study reveals that deaths from dementia in the U.S. have tripled in the past 21 years, rising from around 150,000 in 1999 to over 450,000 in 2020; the likelihood of dying from dementia increased across all demographic groups studied.

Diagnosis

Symptoms are similar across dementia types, and it is difficult to diagnose by symptoms alone. Diagnosis may be aided by brain scanning techniques. In many cases, the diagnosis requires a brain biopsy to become final, but this is rarely recommended (though it can be performed at autopsy). In those who are getting older, general screening for cognitive impairment using cognitive testing or early diagnosis of dementia has not been shown to improve outcomes. However, screening exams are useful in 65+ persons with memory or function complaints.

Normally, symptoms must be present for at least six months to support a diagnosis. Cognitive dysfunction of shorter duration is called delirium. Delirium can be easily confused with dementia due to similar symptoms. Delirium is characterized by a sudden onset, fluctuating course, a short duration (often lasting from hours to weeks), and is primarily related to a somatic (or medical) disturbance. In comparison, dementia has typically a long, slow onset (except in the cases of a stroke or trauma), slow decline of mental functioning, as well as a longer trajectory (from months to years).

Four functional symptoms

Diagnosis of dementia is usually based on medical history and cognitive testing with imaging. Blood tests may be taken to rule out other possible causes that may be reversible, such as hypothyroidism, and to determine the dementia subtype. One commonly used cognitive test is the mini–mental state examination. Although the greatest risk factor for developing dementia is aging, dementia is not a normal part of the aging process; many people aged 90 and above show no signs of dementia. Several risk factors for dementia, such as smoking and obesity, are preventable by lifestyle changes.

Deficits in cognitive function contribute to impaired functional status.[5] The deficits in the domains of cognitive function are[6]:

  • Agnosia - "Failure to recognize or identify objects despite intact sensory function"[6]
  • Aphasia - "Deterioration of language function"[6]
  • Apraxia - "Impaired ability to execute motor activities despite intact motor abilities, sensory function, and comprehension of the required task"[6]
  • Disturbance in executive functioning - "The ability to think abstractly and to plan, initiate, sequence, monitor, and stop complex behavior"[6]

Ascertainment of decision-making capacity

Decision making can be assessed with the Aid to Capacity Evaluation (ACE).[7]

Consequences of labeling

In one study, learning of having mild cognitive impairment reduced stress.[8]

Mental status schedules

Systematic reviews have compared the schedules.[9][6]

A separate systematic review has examined decision making capacity.[7]

Temporal disorientation

Among hospitalized geriatric patients, "failure to identify either year or month correctly was 95% sensitive and 86.5% specific for the detection of cognitive impairment".[10]

Sweet 16

The Sweet 16 is available online at http://hospitalelderlifeprogram.org/private/sweet16-disclaimer.php?pageid=01.09.00. Accuracy using a score of less than 14:[11]

Mini-cog

According to the systematic review by the Rational Clinical Examination, regarding the mini-cog "the performance of the Mini-Cog...cannot be determined with confidence because none of these screens were actually administered in their suggested forms. However, the performance suggested by the retrospective analyses reported in these articles is promising."[6] More recent studies[12] and reviews[13] are favorable. The mini-COG is available at http://www.hospitalmedicine.org/geriresource/toolbox/pdfs/clock_drawing_test.pdf and http://geriatrics.uthscsa.edu/tools/MINICog.pdf .

Mini-mental state examination

The Mini-mental state examination (MMSE) is the most studied test. A systematic review concluded that the accuracy of the MMSE is:

Copies of their MMSE can be purchased (http://www4.parinc.com/Products/Product.aspx?ProductID=MMSE). A copy of the Mini-mental state examination can be found in the appendix of the original publication.[14]

Modified Mini-Mental State examination (3MS)

A meta-analysis concluded that the Modified Mini-Mental State (3MS) examination has:

A copy of the 3MS is online.[15]

Abbreviated mental test score

A meta-analysis concluded:

sensitivity 73% to 100%
specificity 71% to 100%

Clinical Dementia Rating

The Clinical Dementia Rating scale can quantify severity of functional impairment.[16]


St Louis University mental status examination (SLUMS)

The SLUMS has been compared to the MMSE.[17][18] Both evaluations were by the developer of the SLUMS and showed comparable accuracy to the MMSE.

Other examinations

Many other tests have been studied [19][20][21] including the Executive Interview (EXIT)[22].[23]

Investigation of causes

Among rapidly progressive cases, causes include:[24] sporadic, e.g., Creutzfeldt-Jakob disease (sCJD), immunological (vasculitis, encephalomyelitis, and limbic encephalitis), cancer (mainly lymphoma), infectious (fungal, viral, and parasitic), and metabolic (including Wernicke encephalopathy) causes.

Laboratory tests

Apolipoprotein E4

Although apolipoprotein E4 is an important susceptibility gene for Alzheimer's disease[25], its sensitivity and specificity are insufficient (65 and 68 percent, respectively) to be used as a diagnostic test.[26]

Apolipoprotein E4 does not added to other tests in predicting who will develop Alzheimer's.[27]

Treatment

Approaches to treatment

"Actively involving caregivers in making choices about treatments" my be the most important way to delay institutionalization of patients with dementia.[28]

The use of care managers may help.[29][30]

Non drug treatments

Behavior management techniques (BMT)

Behavior management techniques (BMT) might help.[31] More specifically, " interventions that address behavioral issues and unmet needs" may help.[29]

Exercise

Home-based program of physical activity might benefit according to a randomized controlled trial.[32]


Medications

As of 2024, especially regarding Alzheimer's, there are generally no effective medications to either reverse or halt dementia progression. This includes new drugs such as the Alzheimer's anti-beta amyloid monoclonal antibody drug leqembi, which slightly slows the progression of Alzheimer's but does not stop it.

Cholinesterase inhibitors. Available cholinesterase inhibitors drugs are donepezil, galantamine, rivastigmine, and tacrine.

Neuropeptide modifier. Memantine is a neuropeptide modifier that acts on the N-methyl-D-aspartate (NMDA) cell surface receptors for the neurotransmitter glutamate.

Anti-psychotics. The newer, atypical antipsychotic agents (olanzapine, quetiapine, risperidone), were found to have "adverse effects offset advantages in the efficacy of atypical antipsychotic drugs for the treatment of psychosis, aggression, or agitation in patients with Alzheimer's disease."[33] A more recent randomized controlled trial that compared the second generation anti-psychotic agents found that none improved functioning, care needs, or quality of life with statistical significance[33]; however, olanzapine and risperidone may reduce anger.[34] Regardless, antipsychotic agents may increase mortality.[35]

Withdrawing psychotropics agents may prevent accidental falls.[36]

Melatonin. Melatonin may[37]or may not[38][39][40][41] help with associated sleep and behavior disturbance.

Dietary supplements. Ginkgo biloba has conflicting evidence regarding its efficacy.[42][43][44]

Analgesics. Treating pain may reduce agitation.[45]

Prevention

Risk factors for dementia include high blood pressure, high levels of cholesterol, vision loss, hearing loss, smoking, obesity, depression, inactivity, diabetes, lower levels of education, and low social contact. Overindulgence in alcohol, lack of sleep, anemia, traumatic brain injury, and air pollution can also increase the chance of developing dementia. Many of these risk factors, including the lower level of education, smoking, physical inactivity and diabetes, are modifiable. Several of the group are known as vascular risk factors. Managing these risk factors can reduce the risk of dementia in individuals in their late midlife or older age. A reduction in a number of these risk factors, such as switching to a high-fiber, low-fat, plant-based diet or quitting cigarette smoking, can give a positive outcome. The decreased risk achieved by adopting a healthy lifestyle is seen even in those with a high genetic risk.

The standard American diet high in animal products and dairy and concomitant elevated levels of saturated fat is associated with a greater risk of developing dementia. Population and clinical research studies show that plant-based diets low in animal products and high in starch, fruits, and vegetables are associated with lower risk.

Most,[46][47][48][49] but not all[50] studies find that physical activity is associated with reduced risk of dementia. These observational studies cannot prove cause and effect.

Maintaining activities such as cognitive games and reading, playing musical instruments, and physical activities are associated with reduced the risk of dementia in an observational study.[50]

Various medications have been associated with progression or prevention (cholinesterase inhibitors, N-methyl-D-aspartate receptor antagonists, renin-angiotensin system blockers, and hydroxymethylglutaryl-coenzyme A reductase inhibitors) of dementia.[51]

Observational, non-randomized cohort studies suggest that hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) may[52][53] or may not[54][55] prevent dementia.

Ginkgo biloba does not prevent dementia according to a large randomized controlled trial[56] and systematic review[44] by the Cochrane Collaboration in spite of earlier studies that were positive[57].

Screening

Practice guidelines

In 2003, a clinical practice guideline by the U.S. Preventive Services Task Force (USPSTF) gave a grade I recommendation, indicating "the evidence is insufficient to recommend for or against routine screening for dementia in older adults".[58]

Evidence

The late-life dementia risk index:[59]

late-life dementia risk index
Risk Score Incidence of dementia
within 6 years
High ≥8 56%
Intermediate 4-7 23%
Low 0-3 4%
Based on Table 3 from Barnes et al.[59]
  • older age (1–2 points)
  • poor cognitive test performance (2–4 points)
  • body mass index <18.5 (2 points)
  • ≥1 apolipoprotein E 4 alleles (1 point)
  • cerebral MRI findings of white matter disease (1 point)
  • cerebral ventricular enlargement (1 point)
  • internal carotid artery thickening on ultrasonography (1 point)
  • history of coronary artery bypass surgery (1 point)
  • slow physical performance (1 point)
  • lack of alcohol consumption (1 point)

Prognosis

Functional Assessment Staging (FAST) scale[60]
Stage 6
6a = inability to dress
6b = inability to bathe
6c = inability to toilet
6d = urinary incontinence at least occasionally
6e = bowel incontinence at least occasionally
Stage 7
7a = speech is limited to less than 5 words
7b = all intelligible vocabulary is lost
7c = nonambulatory
7d = unable to sit independently
7e = unable to smile
7f = unable to hold head up

Mild cognitive impairment

Mortality is increased with mild cognitive impairment.[61] A systematic review of cohort studies concluded that the rate conversion of mild cognitive impairment to dementia is about 4% per year."[62]

Once a patient has advanced dementia, defined as a score of 5 or 6 on the Cognitive Performance Scale from the most recent Minimum Data Set assessment (a score of 5 corresponds to a score of 5.1 (95% CI: ±10) on the Folstein Mini–Mental State Examination, the median survival is about 18 months.[63]

Dementia

Mortality can also be predicted by Medicare guidelines for use of Hospice. If the patients is a stage 7c on the Functional Assessment Staging (FAST) scale and has had a prior complication of dementia such aspiration pneumonia, stage 4 or more pressure ulcer, upper urinary tract infection, or inability to eat, then mortality is predicted at 6 months with accuracy of:[64]

  • Sensitivity 20%
  • Specificity 89%

Similarly, mortality can be predicted by the ADEPT score.[64]

Legal issues

As of 2024, when improved healthcare means that many people are living longer, there is growing concern about dementia, not just in aging patients but as a result of other health challenges. However, physicians often do not agree among themselves on how to detect and define it. And a medical diagnosis of dementia can have serious legal consequences, resulting (just for example) in a patient losing the right to manage their own finances or make their own medical decisions. Thus, in the U.S., physicians "recommend" that Medicare patients (age 65 and over) be given a cognitive test as part of their annual wellness exam, but they stopped short of requiring such a test.

Attribution

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References

  1. ↑ Wilson H, Pagano G, Politis M (March 2019). "Dementia spectrum disorders: lessons learnt from decades with PET research". J Neural Transm (Vienna). 126(3): 233–251. doi:10.1007/s00702-019-01975-4. PMC 6449308. PMID 30762136.
  2. ↑ McKeith IG, Fairbairn AF, Perry RH, Thompson P (September 1994). "The clinical diagnosis and misdiagnosis of senile dementia of Lewy body type (SDLT)". Br J Psychiatry 165 (3): 324–32. PMID 7994501. [e]
  3. ↑ "Dementia". World Health Organization. Retrieved October 29, 2024.
  4. ↑ Alzheimer's Disease International (September 2015). "World Alzheimer Report 2015" (PDF). Retrieved October 29, 2024.
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  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 Holsinger T, Deveau J, Boustani M, Williams JW (2007). "Does this patient have dementia?". JAMA 297 (21): 2391–404. DOI:10.1001/jama.297.21.2391. PMID 17551132. Research Blogging.
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