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Dementia

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For other uses, see Dementia (disambiguation).
Dementia
SpecialtyPsychiatry, neurology Edit this on Wikidata
Frequency3.8—4% (Asia), 6.1—6.3% (Europe), 6.4—6.6% (Americas), 2.5—2.7% (Africa)

Dementia (meaning "deprived of mind") is a serious cognitive disorder. It may be static, the result of a unique global brain injury or progressive, resulting in long-term decline in cognitive function due to damage or disease in the body beyond what might be expected from normal aging. Although dementia is far more common in the geriatric population, it may occur in any stage of adulthood. This age cutoff is defining, as similar sets of symptoms due to organic brain syndrome or dysfunction, are given different names in populations younger than adult. Up to the end of the nineteenth century, dementia was a much broader clinical concept.[1]

Dementia is a non-specific illness syndrome (set of signs and symptoms) in which affected areas of cognition may be memory, attention, language, and problem solving. It is normally required to be present for at least 6 months to be diagnosed;[2] cognitive dysfunction which has been seen only over shorter times, particularly less than weeks, must be termed delirium. In all types of general cognitive dysfunction, higher mental functions are affected first in the process. Especially in the later stages of the condition, affected persons may be disoriented in time (not knowing what day of the week, day of the month, or even what year it is), in place (not knowing where they are), and in person (not knowing who they are or others around them). Dementia, though often treatable to some degree, is usually due to causes which are progressive and incurable.

Symptoms of dementia can be classified as either reversible or irreversible, depending upon the etiology of the disease. Less than 10 percent of cases of dementia are due to causes which may presently be reversed with treatment. Causes include many different specific disease processes, in the same way that symptoms of organ dysfunction such as shortness of breath, jaundice, or pain are attributable to many etiologies. Without careful assessment of history, the short-term syndrome of delirium (often lasting days to weeks) can easily be confused with dementia, because they have all symptoms in common, save duration, and the fact that delirium is often associated with over-activity of the sympathetic nervous system. Some mental illnesses, including depression and psychosis, may also produce symptoms which must be differentiated from both delirium and dementia.[3] Chronic use of substances such as alcohol can also predispose the patient to cognitive changes suggestive of dementia.

Diagnosis

Proper differential diagnosis between the types of dementia (cortical and subcortical - see below) will require, at the least, referral to a specialist, e.g. a geriatric internist, geriatric psychiatrist, neurologist, neuropsychologist or geropsychologist.[citation needed] However, there exist some brief tests (5–15 minutes) that have reasonable reliability and can be used in the office or other setting to screen cognitive status for deficits which are considered pathological. Examples of such tests include the abbreviated mental test score (AMTS), the mini mental state examination (MMSE), Modified Mini-Mental State Examination (3MS),[4] the Cognitive Abilities Screening Instrument (CASI),[5] and the clock drawing test.[6] An AMTS score of less than six (out of a possible score of ten) and an MMSE score under 24 (out of a possible score of 30) suggests a need for further evaluation. Scores must be interpreted in the context of the person's educational and other background, and the particular circumstances; for example, a person highly depressed or in great pain will not be expected to do well on many tests of mental ability.

Mini-mental state examination

Main article: Mini-mental state examination

The U.S. Preventive Services Task Force (USPSTF) reviewed tests for cognitive impairment and concluded:[7]

  • MMSE
sensitivity 71% to 92%
specificity 56% to 96%

Modified Mini-Mental State examination (3MS)

A copy of the 3MS is online.[8] A meta-analysis concluded that the Modified Mini-Mental State (3MS) examination has:[9]

sensitivity 83% to 93.5%
specificity 85% to 90%

Abbreviated mental test score

Main article: abbreviated mental test score

A meta-analysis concluded:[9]

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

Duration of symptoms

Duration of symptoms must normally exceed 6 months for a diagnosis of dementia or organic brain syndrome to be made.

Other examinations

Many other tests have been studied[10][11][12] including the clock-drawing test (example form). Although some may emerge as better alternatives to the MMSE, presently the MMSE is the best studied. However, access to the MMSE is now limited by enforcement of its copyright.[citation needed]

Another approach to screening for dementia is to ask an informant (relative or other supporter) to fill out a questionnaire about the person's everyday cognitive functioning. Informant questionnaires provide complementary information to brief cognitive tests. Probably the best known questionnaire of this sort is the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE).[13]

The General Practitioner Assessment Of Cognition combines both, a patient assessment and an informant interview. It was specifically designed for the use in the primary care setting and is also available as web-based test. It can be accessed on www.gpcog.com.au.

Further evaluation includes retesting at another date, and administration of other (and sometimes more complex) tests of mental function, such as formal neuropsychological testing.

Laboratory tests

Routine blood tests are also usually performed to rule out treatable causes. These tests include vitamin B12, folic acid, thyroid-stimulating hormone (TSH), C-reactive protein, full blood count, electrolytes, calcium, renal function, and liver enzymes. Abnormalities may suggest vitamin deficiency, infection or other problems that commonly cause confusion or disorientation in the elderly. The problem is complicated by the fact that these cause confusion more often in persons who have early dementia, so that "reversal" of such problems may ultimately only be temporary.

Testing for alcohol and other known dementia-inducing drugs may be indicated.

Imaging

A CT scan or magnetic resonance imaging (MRI scan) is commonly performed, although these modalities do not have optimal sensitivity for the diffuse metabolic changes associated with dementia in a patient who shows no gross neurological problems (such as paralysis or weakness) on neurological exam. CT or MRI may suggest normal pressure hydrocephalus, a potentially reversible cause of dementia, and can yield information relevant to other types of dementia, such as infarction (stroke) that would point at a vascular type of dementia.

The functional neuroimaging modalities of SPECT and PET are more useful in assessing long-standing cognitive dysfunction, since they have shown similar ability to diagnose dementia as a clinical exam.[14] The ability of SPECT to differentiate the vascular cause from the Alzheimer disease cause of dementias, appears to be superior to differentiation by clinical exam.[15]

Recent research has established the value of PET imaging using carbon-11 Pittsburgh Compound B as a contrast medium (PIB-PET) in predictive diagnosis of various kinds of dementia, particularly Alzheimer's disease. Studies from Australia have found PIB-PET to be 86% accurate in predicting which patients with mild cognitive impairment would develop Alzheimer's disease within two years. In another study, carried out using 66 patients seen at the University of Michigan, PET studies using either PIB or another contrast agent, carbon-11 dihydrotetrabenazine (DTBZ), led to more accurate diagnosis for more than one-fourth of patients with mild cognitive impairment or mild dementia.[16]

Types

Cortical dementias

Cortical dementias arise from a disorder affecting the cerebral cortex, the outer layers of the brain that play a critical role in cognitive processes such as memory and language.

Subcortical dementias

Subcortical dementias result from dysfunction in the parts of the brain that are beneath the cortex. Usually, the memory loss and language difficulties that are characteristic of cortical dementias are not present. Rather, people with subcortical dementias, such as Huntington's disease, Parkinson's Disease, and AIDS dementia complex, tend to show changes in their personality and attention span, and their thinking slows down.

Dementia and early onset dementia have been associated with neurovisceral porphyrias. Porphyria is listed in textbooks in the differential diagnosis of dementia. Because acute intermittent porphyria, hereditary coproporphyria and variegate porphyria are aggravated by environmental toxins and drugs the disorders should be ruled out when these etiologies are raised.

Treatment

Except for the treatable types listed above, there is no cure to this illness, although scientists are progressing in making a type of medication that will slow down the process.[citation needed] Cholinesterase inhibitors are often used early in the disease course. Cognitive and behavioral interventions may also be appropriate. Educating and providing emotional support to the caregiver (or carer) is of importance as well (see also elderly care).

A Canadian study found that a lifetime of bilingualism has a marked influence on delaying the onset of dementia by an average of four years when compared to monolingual patients. The researchers determined that the onset of dementia symptoms in the monolingual group occurred at the mean age of 71.4, while the bilingual group was 75.5 years. The difference remained even after considering the possible effect of cultural differences, immigration, formal education, employment and even gender as influences in the results.[18]

Some studies worldwide have found that Music therapy may be useful in helping patients with dementia.[19][20][21][22][23]

Medications

Tacrine (Cognex), donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon) are approved by the United States Food and Drug Administration (FDA) for treatment of dementia induced by Alzheimer disease. They may be useful for other similar diseases causing dementia such as Parkinsons or vascular dementia.[24]

  • N-methyl-D-aspartate Blockers. Memantine (Namenda) is a drug representative of this class. It can be used in combination with acetylcholinesterase inhibitors.[25][26]

Off label

  • Amyloid deposit inhibitors

Minocycline and Clioquinoline, antibiotics, may help reduce amyloid deposits in the brains of persons with Alzheimer disease.[27]

Depression is frequently associated with dementia and generally worsens the degree of cognitive and behavioral impairment. Antidepressants effectively treat the cognitive and behavioral symptoms of depression in patients with Alzheimer's disease,[28] but evidence for their use in other forms of dementia is weak.[29]

Many patients with dementia experience anxiety symptoms. Although benzodiazepines like diazepam (Valium) have been used for treating anxiety in other situations, they are often avoided because they may increase agitation in persons with dementia and are likely to worsen cognitive problems or are too sedating. Buspirone (Buspar) is often initially tried for mild-to-moderate anxiety.[citation needed] There is little evidence for the effectiveness of benzodiazepines in dementia whereas there is evidence for the effectivess of antipsychotics (at low doses).[30]

Selegiline, a drug used primarily in the treatment of Parkinson's disease, appears to slow the development of dementia. Selegiline is thought to act as an antioxidant, preventing free radical damage. However, it also acts as a stimulant, making it difficult to determine whether the delay in onset of dementia symptoms is due to protection from free radicals or to the general elevation of brain activity from the stimulant effect.[31]

  • Antipsychotic drugs

Both typical antipsychotics (such as Haloperidol) and atypical antipsychotics such as (risperidone) increases the risk of death in dementia-associated psychosis.[32] This means that any use of antipsychotic medication for dementia-associated psychosis is off-label and should only be considered after discussing the risks and benefits of treatment with these drugs, and after other treatment modalities have failed.

Prevention

Main article: Prevention of dementia

It appears that the regular moderate consumption of alcohol (beer, wine, or distilled spirits) and a Mediterranean diet may reduce risk.[33][34][35][36] A study has shown a link between high blood pressure and developing dementia. The study, published in the Lancet Neurology journal July 2008, found that blood pressure lowering medication reduced dementia by 13%.[37][38]

Brain-derived neurotrophic factor (BDNF) expression is associated with some dementia types.[39][40][41]

NSAIDs

Non-steroidal anti-inflammatory drugs (NSAIDs) can decrease the risk of developing Alzheimer's and Parkinson's diseases.[42] Research into the use of NSAID pain relievers has been going on for decades, but it is unlikely to ever be recommended, due to the fact that most NSAIDs are off patent and can be made very cheaply. The length of time needed to prevent dementia varies, but in most studies it is usually between 2 and 10 years. [43] [44] [45] [46] [47]

Research has also shown that it must be used in clinically relevant dosages and that so called "baby aspirin" doses are ineffective at preventing and treating dementia. [48]

Alzheimer's disease causes inflammation in the neurons by its deposits of amyloid beta peptides and neurofibrillary tangles. These deposits irritate the body by causing a release of e.g. cytokines and acute phase proteins, leading to inflammation. When these substances accumulate over years they contribute to the effects of Alzheimer's.[49] NSAIDs inhibit the formation of such inflammatory substances, and prevent the deteriorating effects.[50] [51] [52]

Comorbidities

Dementia is not merely a problem of memory. Additional mental and behavioral problems often affect people who have dementia, and may influence quality of life, caregivers, and the need for institutionalization.

Depression affects 20-30% of people who have dementia, and about 20% have anxiety.[53] Psychosis (often delusions of persecution) and agitation/aggression also often accompany dementia. Each of these needs to be assessed and treated independent of the underlying dementia. [54]

Risk to self and others

The Canadian Medical Association Journal has reported that driving with dementia could lead to severe injury or even death to self and others. Doctors should advise appropriate testing on when to quit driving.[55]

In the United States, Florida's Baker Act allows law enforcement and the judiciary to force mental evaluation for those suspected of suffering from dementia or other mental incapacities.[citation needed]

In the United Kingdom, as with all mental disorders, where a sufferer could potentially be a danger to themselves or others, they can be detained under the Mental Health Act 1983 for the purposes of assessment, care and treatment. This is a last resort, and usually avoided if the patient has family or friends who can ensure care.

The United Kingdom DVLA (Driving & Vehicle Licensing Agency) states that Dementia sufferers who specifically suffer with poor short term memory, disorientation, lack of insight or judgement are almost certainly not fit to drive - and in these instances, the DVLA must be informed so said license can be revoked. They do however acknowledge low-severity cases and early sufferers, and those drivers may be permitted to drive pending medical report.

Services

Adult daycare centers as well as special care units in nursing homes often provide specialized care for dementia patients. Adult daycare centers offer supervision, recreation, meals, and limited health care to participants, as well as providing respite for caregivers.

See also

References

Notes

  1. ^ Berrios GE (1987). "Dementia during the seventeenth and eighteenth centuries: a conceptual history". Psychological Medicine. 17 (4): 829–37. ISSN 0033-2917. PMID 3324141. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)
  2. ^ "Dementia definition". MDGuidelines. Reed Group. Retrieved 2009-06-04.
  3. ^ Gleason OC (2003). "Delirium". American Family Physician. 67 (5): 1027–34. PMID 12643363. Retrieved 2009-06-04. {{cite journal}}: Unknown parameter |month= ignored (help)
  4. ^ Teng EL, Chui HC (1987). "The Modified Mini-Mental State (3MS) examination". The Journal of Clinical Psychiatry. 48 (8): 314–8. ISSN 0160-6689. PMID 3611032. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)
  5. ^ Teng EL, Hasegawa K, Homma A; et al. (1994). "The Cognitive Abilities Screening Instrument (CASI): a practical test for cross-cultural epidemiological studies of dementia". International Psychogeriatrics / IPA. 6 (1): 45–58, discussion 62. doi:10.1017/S1041610294001602. PMID 8054493. {{cite journal}}: |access-date= requires |url= (help); Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  6. ^ Royall, D.; Cordes J.; & Polk M. (1998). "CLOX: an executive clock drawing task". J Neurol Neurosurg Psychiatry. 64 (5): 588–94. doi:10.1136/jnnp.64.5.588. PMID 9598672.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Boustani, M.; Peterson, B.; Hanson, L.; Harris, R.; & Lohr, K. (2003). "Screening for dementia in primary care: a summary of the evidence for the U.S. Preventive Services Task Force". Ann Intern Med. 138 (11): 927–37. PMID 12779304. {{cite journal}}: Unknown parameter |day= ignored (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ "Appendix: The Modified Mini-Mental State (3MS)". Retrieved 2007-09-06.
  9. ^ a b Cullen B, O'Neill B, Evans JJ, Coen RF, Lawlor BA (2007). "A review of screening tests for cognitive impairment". Journal of Neurology, Neurosurgery, and Psychiatry. 78 (8): 790–9. doi:10.1136/jnnp.2006.095414. PMID 17178826. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ Sager MA, Hermann BP, La Rue A, Woodard JL (2006). "Screening for dementia in community-based memory clinics" (PDF). WMJ : Official Publication of the State Medical Society of Wisconsin. 105 (7): 25–9. PMID 17163083. Retrieved 2009-06-04. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  11. ^ Fleisher, A.; Sowell B.; Taylor C.; Gamst A.; Petersen R.; & Thal L. (2007). "Clinical predictors of progression to Alzheimer disease in amnestic mild cognitive impairment". Neurology. 68: 1588. doi:10.1212/01.wnl.0000258542.58725.4c. PMID 17287448.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Karlawish, J. & Clark, C. (2003). "Diagnostic evaluation of elderly patients with mild memory problems". Ann Intern Med. 138 (5): 411–9. PMID 12614094.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Jorm AF (2004). "The Informant Questionnaire on cognitive decline in the elderly (IQCODE): a review". International Psychogeriatrics / IPA. 16 (3): 275–93. doi:10.1017/S1041610204000390. PMID 15559753. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)
  14. ^ Bonte, FJ (2006). "Tc-99m HMPAO SPECT in the differential diagnosis of the dementias with histopathologic confirmation". Clinical Nuclear Medicine. 31 (7): 376–8. doi:10.1097/01.rlu.0000222736.81365.63. PMID 16785801. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  15. ^ Dougall, NJ (2004). "Systematic review of the diagnostic accuracy of 99mTc-HMPAO-SPECT in dementia". The American Journal of Geriatric Psychiatry. 12 (6): 554–70. doi:10.1176/appi.ajgp.12.6.554. PMID 15545324. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  16. ^ Abella HA (June 16, 2009). "Report from SNM: PET imaging of brain chemistry bolsters characterization of dementias". Diagnostic Imaging.
  17. ^ Boyles, Salynn. Celiac Disease Linked to Dementia. http://www.webmd.com/news/20061013/celiac-disease-linked-dementia
  18. ^ "Bilingualism Has Protective Effect In Delaying Onset Of Dementia By Four Years, Canadian Study Shows". Medical News Today. 2007-01-11. Retrieved 2007-01-16.
  19. ^ Aldridge, David, Music Therapy in Dementia Care, London : Jessica Kingsley Publishers, November 2000. ISBN 1853027766
  20. ^ Tuet, R.W.K.; Lam, L.C.W. (September 2006) "A preliminary study of the effects of music therapy on agitation in Chinese patients with dementia", Hong Kong Journal of Psychiatry, Volume 16, Number 3
  21. ^ Watanabe, Tomoyuki; et al., "Effects of music therapy for dementia: A systematic review", (in Japanese) Aichi University of Education Research Reports, v.55, pp. 57-61, March, 2005
  22. ^ Koger, Susan M.; Chapin Kathyn; Brotons, Melissa, "Is Music Therapy an Effective Intervention for Dementia? : A Meta-Analytic Review of Literature", Journal of Music Therapy 36(1), February 1999, pp.2-15.
  23. ^ Remington, Ruth, "Calming Music and Hand Massage With Agitated Elderly", Nursing Research 51(5): 317-323, September/October 2002.
  24. ^ Lleo A, Greenberg SM, Growdon JH. Current pharmacotherapy for Alzheimer's disease. Annu Rev Med. 2006;57:513-33. Review. PMID 16409164
  25. ^ Raina P, Santaguida P, Ismaila A; et al. (2008). "Effectiveness of cholinesterase inhibitors and memantine for treating dementia: evidence review for a clinical practice guideline". Annals of Internal Medicine. 148 (5): 379–97. PMID 18316756. Retrieved 2009-06-04. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  26. ^ Atri A, Shaughnessy LW, Locascio JJ, Growdon JH (2008). "Long-term course and effectiveness of combination therapy in Alzheimer disease". Alzheimer Disease and Associated Disorders. 22 (3): 209–21. doi:10.1097/WAD.0b013e31816653bc. PMID 18580597. {{cite journal}}: |access-date= requires |url= (help)CS1 maint: multiple names: authors list (link)
  27. ^ Choi Y, Kim HS, Shin KY; et al. (2007). "Minocycline attenuates neuronal cell death and improves cognitive impairment in Alzheimer's disease models". Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology. 32 (11): 2393–404. doi:10.1038/sj.npp.1301377. PMID 17406652. {{cite journal}}: |access-date= requires |url= (help); Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  28. ^ Thompson S, Herrmann N, Rapoport MJ, Lanctôt KL (2007). "Efficacy and safety of antidepressants for treatment of depression in Alzheimer's disease: a metaanalysis" (PDF). Canadian Journal of Psychiatry. Revue Canadienne De Psychiatrie. 52 (4): 248–55. PMID 17500306. Retrieved 2009-06-04. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  29. ^ Bains J, Birks JS, Dening TR (2002). "The efficacy of antidepressants in the treatment of depression in dementia". Cochrane Database of Systematic Reviews (Online) (4): CD003944. doi:10.1002/14651858.CD003944. PMID 12519625. {{cite journal}}: |access-date= requires |url= (help)CS1 maint: multiple names: authors list (link)
  30. ^ Lolk A, Gulmann NC (2006). "[Psychopharmacological treatment of behavioral and psychological symptoms in dementia]". Ugeskr Laeg (in Danish). 168 (40): 3429–32. PMID 17032610.
  31. ^ Riederer P, Lachenmayer L (2003). "Selegiline's neuroprotective capacity revisited". Journal of Neural Transmission (Vienna, Austria : 1996). 110 (11): 1273–8. doi:10.1007/s00702-003-0083-x. PMID 14628191. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)
  32. ^ "FDA MedWatch - 2008 Safety Alerts for Human Medical Products". FDA.
  33. ^ Mukamal KJ, Kuller LH, Fitzpatrick AL, Longstreth WT, Mittleman MA, Siscovick DS (2003). "Prospective study of alcohol consumption and risk of dementia in older adults". JAMA. 289 (11): 1405–13. doi:10.1001/jama.289.11.1405. PMID 12636463. {{cite journal}}: Unknown parameter |doi_brokendate= ignored (|doi-broken-date= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  34. ^ Ganguli M, Vander Bilt J, Saxton JA, Shen C, Dodge HH (2005). "Alcohol consumption and cognitive function in late life: a longitudinal community study". Neurology. 65 (8): 1210–7. doi:10.1212/01.wnl.0000180520.35181.24. PMID 16247047. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  35. ^ Huang W, Qiu C, Winblad B, Fratiglioni L (2002). "Alcohol consumption and incidence of dementia in a community sample aged 75 years and older". J Clin Epidemiol. 55 (10): 959–64. doi:10.1016/S0895-4356(02)00462-6. PMID 12464371. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  36. ^ Sofi F, Cesari F, Abbate R, Gensini GF, Casini A (2008). "Adherence to Mediterranean diet and health status: meta-analysis". BMJ. 337: a1344. doi:10.1136/bmj.a1344. PMC 2533524. PMID 18786971.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Fillit H, Nash DT, Rundek T, Zuckerman A (2008). "Cardiovascular risk factors and dementia". Am J Geriatr Pharmacother. 6 (2): 100–18. doi:10.1016/j.amjopharm.2008.06.004. PMID 18675769. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  38. ^ Peters R, Beckett N, Forette F; et al. (2008). "Incident dementia and blood pressure lowering in the Hypertension in the Very Elderly Trial cognitive function assessment (HYVET-COG): a double-blind, placebo controlled trial". Lancet Neurol. 7 (8): 683–9. doi:10.1016/S1474-4422(08)70143-1. PMID 18614402. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  39. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 18208542, please use {{cite journal}} with |pmid=18208542 instead.
  40. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 18184369, please use {{cite journal}} with |pmid=18184369 instead.
  41. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1016/j.brainresrev.2008.07.007, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1016/j.brainresrev.2008.07.007 instead.
  42. ^ West Virginia Department of Health and Human Resources (with further links to experiments respectively)
  43. ^ http://www.ncbi.nlm.nih.gov/pubmed/18509093?ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
  44. ^ http://www.ncbi.nlm.nih.gov/pubmed/15084783?ordinalpos=46&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
  45. ^ http://www.bmj.com/cgi/content/full/327/7407/128?view=long&pmid=12869452
  46. ^ http://preview.ncbi.nlm.nih.gov/pubmed/12827329?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=58
  47. ^ http://preview.ncbi.nlm.nih.gov/pubmed/10851364?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=90
  48. ^ http://www.ncbi.nlm.nih.gov/pubmed/18068522?ordinalpos=20&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
  49. ^ Inflammation and Alzheimer's disease, Neurobiol Aging. 2000 May-Jun;21(3):383-421
  50. ^ http://www.ncbi.nlm.nih.gov/pubmed/16386371?ordinalpos=32&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
  51. ^ http://www.ncbi.nlm.nih.gov/pubmed/16125740?ordinalpos=37&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
  52. ^ http://preview.ncbi.nlm.nih.gov/pubmed/11711868?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=78
  53. ^ Calleo J, Stanley M (2008). "Anxiety Disorders in Later Life Differentiated Diagnosis and Treatment Strategies". Psychiatric Times. 25 (8). {{cite journal}}: line feed character in |title= at position 32 (help)
  54. ^ Shub, Denis; Kunik, Mark E (April 16, 2009). "Psychiatric Comorbidity in Persons With Dementia: Assessment and Treatment Strategies". Psychiatric Times. 26 (4).{{cite journal}}: CS1 maint: date and year (link)
  55. ^ Drivers with dementia a growing problem, MDs warn, CBC News, Canada, September 19, 2007

External links


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