Alzheimer's disease: Difference between revisions

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==Treatment==
==Treatment==


:'''Medical:''' [[Alzheimer's disease medical therapy| Medical Therapy]]
:'''Medical:''' [[Alzheimer's disease medical therapy| Medical Therapy]] | [[Alzheimer's disease primary prevention|Prevention]]


:'''Surgical:''' [[Alzheimer's disease surgery| Surgery]]
:'''Surgical:''' [[Alzheimer's disease surgery| Surgery]]

Revision as of 13:46, 16 August 2012

Template:DiseaseDisorder infobox

Alzheimer's disease Microchapters

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Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1] Phone:617-632-7753; Peter Pressman, M.D. [2], Northwestern Memorial Hospital, Department of Neurology

Dr. Pressman has nothing to disclose.

Synonyms and keywords: AD; Alzheimer disease; senile dementia of the Alzheimer type; SDAT; Alzheimer's

Overview

Historical Perspective

Classification

Pathophysiology

Epidemiology and Demographics

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms | Physical Examination | Lab Studies | Electrocardiogram | Chest X Ray | MRI | CT | Echocardiography | Other imaging findings

Treatment

Medical: Medical Therapy | Prevention
Surgical: Surgery

Background

Alzheimer's disease (AD), also called Alzheimer disease, Senile Dementia of the Alzheimer Type (SDAT) or simply Alzheimer's, is the most common form of dementia.

Although each sufferer experiences Alzheimer's in a unique way, there are many common symptoms.[1] The earliest observable symptoms are often mistakenly thought to be 'age-related' changes, or manifestations of stress.[2] The most commonly recognized symptom of early Alzheimer's disease is memory loss, usually the forgetting of recently learned facts. As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline.[2][3] Gradually, bodily functions are lost, ultimately leading to death.[4] When a doctor or physician has been notified, and AD is suspected, the diagnosis is usually further supported by behavioral assessments and cognitive tests, often followed by a brain scan if available.[5] Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years.[6] Fewer than three percent of individuals live more than fourteen years after diagnosis.[7]

The cause of Alzheimer's disease is poorly understood. Research indicates that the disease is associated with plaques and tangles in the brain.[8] Currently-used treatments offer a small symptomatic benefit. No treatments to halt the progression of the disease are yet available. As of 2010, more than 700 clinical trials were investigating possible treatments for AD, but it is unknown if any of them will prove successful.[9] Many measures have been suggested for the prevention of Alzheimer's disease, but the value of these measures is unproven in slowing the course and reducing the severity of the disease. Mental stimulation, exercise, and a balanced diet are often recommended as both a possible prevention and a sensible way of managing the disease.[10]

Because AD cannot be cured, management of patients is essential as the disease progresses. The role of the main caregiver is often taken by a spouse or a close relative.[11] Alzheimer's disease is known for placing a great burden on caregivers; the pressures can be wide-ranging, affecting social, psychological, physical, and economic components of the caregiver's life.[12][13][14] In developed countries, AD is one of the most economically costly diseases to society.[15][16]

Prevention

Intellectual activities such as playing chess or regular social interaction have been linked to a reduced risk of AD in epidemiological studies, although no causal relationship has been found.

Specific measures to delay or prevent the onset of AD are lacking. This is due to contradictory results in global studies, as well as a paucity of proven causal relationships between risk factors and the disease.[17] Modifiable factors such as diet, cardiovascular risks, pharmaceutical products, or intellectual activities have all been evaluated with epidemiological studies to see if they increase a population's risk of developing AD.[18]

The components of a Mediterranean diet, which include fruit and vegetables, bread, wheat and other cereals, olive oil, fish, and red wine, may reduce the risk and course of Alzheimer's disease. There is evidence that frequent and moderate consumption of alcohol (beer, wine or distilled spirits) reduces the risk of the disease,[19] [20] but it is still considered premature to make dietary recommendations on this basis.[21][22] Vitamins E, B, and C, or folic acid have appeared to be related to a reduced risk of AD,[23] but other studies indicate that they do not have any significant effect on the onset or course of the disease, but may have important secondary effects in conjunction with other therapies.[24] Curcumin in curry has shown some effectiveness in preventing brain damage in mouse models.[25]

Although cardiovascular risk factors, such as hypercholesterolemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and course of AD,[26][27] statins, which are cholesterol lowering drugs, have not been effective in preventing or improving the course of the disease.[28][29] However long-term usage of non-steroidal anti-inflammatory drug (NSAIDs), is associated with a reduced likelihood of developing AD in some individuals.[30][31][32]

Other pharmaceutical therapies such as female hormone replacement therapy are no longer thought to prevent dementia,[33][34] and a 2007 systematic review concluded that there was inconsistent and unconvincing evidence that ginkgo has any positive effect on dementia or cognitive impairment.[35]

Intellectual activities such as playing chess, completing crossword puzzles or regular social interaction may also delay the onset or reduce the severity of Alzheimer's disease.[36][37] Bilingualism is also related to a later onset of Alzheimer's disease.[38]

Management

There is no known cure for Alzheimer's disease. Available treatments offer relatively small symptomatic benefit but remain palliative in nature. Current treatments can be divided into pharmaceutical, psychosocial and caregiving.

Psychosocial intervention

A specifically designed room for sensory integration therapy, or snoezelen; an emotion-oriented psychosocial intervention for people with dementia

Psychosocial interventions are used as an adjunct to pharmaceutical treatment and can be classified within behavior, emotion, cognition or stimulation oriented approaches. Research on efficacy is unavailable and rarely specific to Alzheimer's disease, focusing instead on dementia as a whole.[39]

Behavioral interventions attempt to identify and reduce the antecedents and consequences of problem behaviors. This approach has not shown success in the overall functioning of patients,[40] but can help to reduce some specific problem behaviors, such as incontinence.[41] There is still a lack of high quality data on the effectiveness of these techniques in other behavior problems such as wandering.[42][43]

Emotion-oriented interventions include reminiscence therapy, validation therapy, supportive psychotherapy, sensory integration or snoezelen, and simulated presence therapy. Supportive psychotherapy has received little or no formal scientific study, but some clinicians find it useful in helping mildly impaired patients adjust to their illness.[39] Reminiscence therapy (RT) involves the discussion of past experiences individually or in group, often with the aid of photographs, household items, music and sound recordings, or other familiar items from the past. Although there are few quality studies on the effectiveness of RT it may be beneficial for cognition and mood.[44] Simulated presence therapy (SPT) is based on attachment theories and is normally carried out playing a recording with voices of the closest relatives of the patient. There is preliminary evidence indicating that SPT may reduce anxiety and challenging behaviors.[45][46] Finally, validation therapy is based on acceptance of the reality and personal truth of another's experience, while sensory integration is based on exercises aimed to stimulate senses. There is little evidence to support the usefulness of these therapies.[47][48]

The aim of cognition-oriented treatments, which include reality orientation and cognitive retraining is the restoration of cognitive deficits. Reality orientation consists of the presentation of information about time, place or person in order to ease the the patient's understanding of their surroundings. On the other hand, cognitive retraining tries to improve impaired capacities by exercising mental abilities. Both have shown some efficacy improving cognitive capacities,[49][50] although in some works these effects were transient. Negative effects, such as frustration, have also been reported.[39]

Stimulation-oriented treatments include art, music and pet therapies, exercise, and any other kind of recreational activities for patients. Stimulation has modest support for improving behavior, mood, and, to a lesser extent, function. Nevertheless, as important as these effects are, the main support for the use of stimulation therapies is the improvement in the patient's daily life, as opposed to improving the underlying disease course.[39]

Caregiving

Further information: [[:Caregiving and dementia]]

Since there is no cure for Alzheimer's, caregiving is an essential part of the treatment. Due to the eventual inability for the sufferer to self-care, Alzheimer's has to be carefully care-managed. Home care in the familiar surroundings of home may delay onset of some symptoms and delay or eliminate the need for more professional and costly levels of care.[51] Many family members choose to look after their relative,[52] but two-thirds of nursing home residents have dementias.[53]

Modifications to the living environment and lifestyle of the Alzheimer's patient can improve functional performance and ease caretaker burden. Assessment by an occupational therapist is often indicated. Adherence to simplified routines and labeling of household items to cue the patient can aid with activities of daily living, while placing safety locks on cabinets, doors, and gates and securing hazardous chemicals can prevent accidents and wandering. Changes in routine or environment can trigger or exacerbate agitation, whereas well-lit rooms, adequate rest, and avoidance of excess stimulation all help prevent such episodes.[54][55] Appropriate social and visual stimulation can improve function by increasing awareness and orientation. For instance, boldly colored tableware aids those with severe AD, helping people overcome a diminished sensitivity to visual contrast to increase food and beverage intake.[56]

Clinical research

Main article: Alzheimer's disease clinical research

As of 2008, the safety and efficacy of more than 400 pharmaceutical treatments are being investigated in clinical trials worldwide, and approximately one-fourth of these compounds are in Phase III trials, which is the last step prior to review by regulatory agencies.[57] It is unknown as to whether any of these trials will ultimately prove successful in treating the disease.

A critical area of clinical research is focused on treating the underlying disease pathology. Reduction of amyloid beta levels is a common target of compounds under investigation. Immunotherapy or vaccination for the amyloid protein is one treatment modality under study. Unlike vaccines which seek to prevent disease, this therapy would be used to treat diagnosed patients, and is based upon the concept of training the immune system to recognize, attack, and reverse deposition of amyloid, thereby altering the course of the disease.[58] An example of such a vaccine under investigation is ACC-001.[59][60] Similar agents are bapineuzumab, an antibody designed as identical to the naturally-induced anti-amyloid antibody,[61] and MPC-7869, a selective amyloid beta-42 lowering agent.[62] Other approaches are neuroprotective agents, such as AL-108,[63] metal-protein interaction attenuation agents, such as PBT2,[64] or tumor necrosis factor-alpha receptor fusion proteins, such as etanercept.[65][66][67] There are also many basic investigations attempting to increase the knowledge on the origin and mechanisms of the disease that may lead to new treatments.

Society and culture

Social costs

Because the median age of the industrialised world's population is gradually increasing, Alzheimer's is a major public health challenge. Much of the concern about the solvency of governmental social safety nets is founded on estimates of the costs of caring for baby boomers, assuming that they develop Alzheimer's in the same proportions as earlier generations. For this reason, money spent informing the public of available effective prevention methods may yield disproportionate benefits.[68]

Caregiving burden

Further information: [[:Caregiving and dementia]]

The role of family caregivers has become more prominent in both reducing the social cost of care and improving the quality of life of the patient. Home-based care also can have economic, emotional, and psychological costs to the patient's family. Although family members in particular often express the desire to care for the sufferer to the end,[69] Alzheimer's disease is known for effecting a high burden on caregivers.[52]

Alzheimer's disease can incur a variety of stresses on the caregivers: typical complaints are stress, depression, and an inability to cope. Reasons for these complaints can include: high-demands on the caregiver's concentration, as Alzheimer's sufferers have a decreasing regard for their own safety (and can wander when unattended, for example); the lack of gratitude received when the sufferer is unaware of the help being given; and the lack of satisfaction when the sufferer's condition does not abate. Alzheimer's sufferers can be verbally and physically aggressive, and can stubbornly refuse to be helped. Aggression in particular can lead to a temptation to retaliate, which can put both the sufferer and carer at risk. It is additionally stressful for caregivers who are friends and family to witness a sufferer lose his or her identity, and eventually be unable to recognise them.[52]

Family caregivers often give up time from work and forego pay to spend 47 hours per week on average with the person with AD. From a 2006 survey of US patients with long term care insurance, direct and indirect costs of caring for an Alzheimer's patient average $77,500 per year.[70]


References

  1. ↑ "What is Alzheimer's disease?". Alzheimers.org.uk. 2007. Retrieved 2008-02-21. Unknown parameter |month= ignored (help)
  2. ↑ 2.0 2.1 Waldemar G, Dubois B, Emre M; et al. (2007). "Recommendations for the diagnosis and management of Alzheimer's disease and other disorders associated with dementia: EFNS guideline". Eur. J. Neurol. 14 (1): e1–26. doi:10.1111/j.1468-1331.2006.01605.x. PMID 17222085. Unknown parameter |month= ignored (help)
  3. ↑ Tabert MH, Liu X, Doty RL, Serby M, Zamora D, Pelton GH, Marder K, Albers MW, Stern Y, Devanand DP (2005). "A 10-item smell identification scale related to risk for Alzheimer's disease". Ann. Neurol. 58 (1): 155–160. doi:10.1002/ana.20533. PMID 15984022.
  4. ↑ "Understanding stages and symptoms of Alzheimer's disease". National Institute on Aging. 2007-10-26. Retrieved 2008-02-21.
  5. ↑ "Alzheimer's diagnosis of AD". Alzheimer's Research Trust. Retrieved 2008-02-29.
  6. ↑ Mölsä PK, Marttila RJ, Rinne UK (1986). "Survival and cause of death in Alzheimer's disease and multi-infarct dementia". Acta Neurol. Scand. 74 (2): 103–7. PMID 3776457. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  7. ↑ Mölsä PK, Marttila RJ, Rinne UK (1995). "Long-term survival and predictors of mortality in Alzheimer's disease and multi-infarct dementia". Acta Neurol. Scand. 91 (3): 159–64. PMID 7793228. Unknown parameter |month= ignored (help)
  8. ↑
  9. ↑ "Alzheimer's Disease Clinical Trials". US National Institutes of Health. Retrieved 2008-08-18.
  10. ↑ "Can Alzheimer's disease be prevented" (pdf). National Institute on Aging. 2006-08-29. Retrieved 2008-02-29.
  11. ↑ "The MetLife study of Alzheimer's disease: The caregiving experience" (PDF). MetLife Mature Market Institute. 2006. Retrieved 2008-02-12. Unknown parameter |month= ignored (help)
  12. ↑ Thompson CA, Spilsbury K, Hall J, Birks Y, Barnes C, Adamson J (2007). "Systematic review of information and support interventions for caregivers of people with dementia". BMC Geriatr. 7: 18. doi:10.1186/1471-2318-7-18. PMC 1951962. PMID 17662119.
  13. ↑ Schneider J, Murray J, Banerjee S, Mann A (1999). "EUROCARE: a cross-national study of co-resident spouse carers for people with Alzheimer's disease: I—Factors associated with carer burden". International Journal of Geriatric Psychiatry. 14 (8): 651–661. doi:10.1002/(SICI)1099-1166(199908)14:8<651::AID-GPS992>3.0.CO;2-B. PMID 10489656. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  14. ↑ Murray J, Schneider J, Banerjee S, Mann A (1999). "EUROCARE: a cross-national study of co-resident spouse carers for people with Alzheimer's disease: II--A qualitative analysis of the experience of caregiving". International Journal of Geriatric Psychiatry. 14 (8): 662–667. doi:10.1002/(SICI)1099-1166(199908)14:8<662::AID-GPS993>3.0.CO;2-4. PMID 10489657. Unknown parameter |month= ignored (help)
  15. ↑ Bonin-Guillaume S, Zekry D, Giacobini E, Gold G, Michel JP (2005). "Impact économique de la démence (English: The economical impact of dementia)". Presse Med (in French). 34 (1): 35–41. ISSN 0755-4982. PMID 15685097. Unknown parameter |month= ignored (help)
  16. ↑ Meek PD, McKeithan K, Schumock GT (1998). "Economic considerations in Alzheimer's disease". Pharmacotherapy. 18 (2 Pt 2): 68–73, discussion 79–82. PMID 9543467.
  17. ↑ Prevention recommendations not supported:
    • Kawas CH (2006). "Medications and diet: protective factors for AD?". Alzheimer Dis Assoc Disord. 20 (3 Suppl 2): S89–96. PMID 16917203.
    • Luchsinger JA, Mayeux R (2004). "Dietary factors and Alzheimer's disease". Lancet Neurol. 3 (10): 579–87. doi:10.1016/S1474-4422(04)00878-6. PMID 15380154.
    • Luchsinger JA, Noble JM, Scarmeas N (2007). "Diet and Alzheimer's disease". Curr Neurol Neurosci Rep. 7 (5): 366–72. doi:10.1007/s11910-007-0057-8. PMID 17764625.
  18. ↑ Szekely CA, Breitner JC, Zandi PP (2007). "Prevention of Alzheimer's disease". Int Rev Psychiatry. 19 (6): 693–706. doi:10.1080/09540260701797944. PMID 18092245.
  19. ↑ Alcohol:
    • Mulkamal KJ; et al. (2003-03-19). "Prospective study of alcohol consumption and risk of dementia in older adults". Journal of the American Medical Association. 289: 1405–1413.
    • Ganguli M; et al. (2005). "Alcohol consumption and cognitive function in late life: A longitudinal community study". Neurology. 65: 1210–1217.
    • Huang W; et al. (2002). "Alcohol consumption and incidence of dementia in a community sample aged 75 years and older". Journal of Clinical Epidemiology. 55 (10): 959–964.
    • Rodgers B; et al. (2005). "Non-linear relationships between cognitive function and alcohol consumption in young, middle-aged and older adults: The PATH Through Life Project". Addiction. 100 (9): 1280–1290.
    • Anstey KJ; et al. (2005). "Lower cognitive test scores observed in alcohol are associated with demographic, personality, and biological factors: The PATH Through Life Project". Addiction. 100 (9): 1291–1301, .Espeland, M.; et al. (2006). "Association between alcohol intake and domain-specific cognitive function in older women". Neuroepidemiology. 1 (27): 1–12.
    • Stampfer MJ; et al. (2005). "Effects of moderate alcohol consumption on cognitive function in women". New England Journal of Medicine. 352: 245–253.
    • Ruitenberg A; et al. (2002). "Alcohol consumption and risk of dementia: the Rotterdam Study". Lancet. 359 (9303): 281–286.
    • Scarmeas N; et al. (2006-04-18). "Mediterranean diet and risk for Alzheimer's disease". Annals of Neurology.
  20. ↑ Mediterranean diet:
    • Scarmeas N, Stern Y, Mayeux R, Luchsinger JA (2006). "Mediterranean diet, Alzheimer disease, and vascular mediation". Arch. Neurol. 63 (12): 1709–1717. doi:10.1001/archneur.63.12.noc60109. PMID 17030648.
    • Scarmeas N, Luchsinger JA, Mayeux R, Stern Y (2007). "Mediterranean diet and Alzheimer disease mortality". Neurology. 69 (11): 1084–93. doi:10.1212/01.wnl.0000277320.50685.7c. PMID 17846408.
    • Barberger-Gateau P, Raffaitin C, Letenneur L, Berr C, Tzourio C, Dartigues JF, Alpérovitch A (2007). "Dietary patterns and risk of dementia: the Three-City cohort study". Neurology. 69 (20): 1921–1930. doi:10.1212/01.wnl.0000278116.37320.52. PMID 17998483.
    • Dai Q, Borenstein AR, Wu Y, Jackson JC, Larson EB (2006). "Fruit and vegetable juices and Alzheimer's disease: the Kame Project". American Journal of Medicine. 119 (9): 751–759. doi:10.1016/j.amjmed.2006.03.045. PMID 16945610.
    • Savaskan E, Olivieri G, Meier F, Seifritz E, Wirz-Justice A, Müller-Spahn F (2003). "Red wine ingredient resveratrol protects from beta-amyloid neurotoxicity". Gerontology. 49 (6): 380–383. doi:10.1159/000073766. PMID 14624067.
  21. ↑ Luchsinger JA, Mayeux R (2004 Oct). "Dietary factors and Alzheimer's disease". Lancet Neurology. 3 (10): 579–587. PMID 15380154. Available data do not permit definitive conclusions regarding diet and AD or specific recommendations on diet modification for the prevention of AD. Check date values in: |date= (help)
  22. ↑ Kawas CH (2006 Jul-Sep). "Medications and diet: protective factors for AD?". Alzheimer Dis Assoc Disord. 20 (3 Suppl 2): S89–96. PMID 16917203. Evidence regarding dietary and supplemental intake of vitamins E, C, and folate, and studies of alcohol and wine intake are also reviewed. At present, there is insufficient evidence to make public health recommendations, but these studies can provide potentially important clues and new avenues for clinical and laboratory research. Check date values in: |date= (help)
  23. ↑ Vitamins:
    • Morris MC, Schneider JA, Tangney CC (2006). "Thoughts on B-vitamins and dementia". J. Alzheimers Dis. 9 (4): 429–33. PMID 16917152.
    • Alzheimer's Association. "Vitamin E".
    • Landmark K (2006). "[Could intake of vitamins C and E inhibit development of Alzheimer dementia?]". Tidsskr. Nor. Laegeforen. (in Norwegian). 126 (2): 159–61. PMID 16415937.
    • Luchsinger JA, Tang MX, Miller J, Green R, Mayeux R (2007). "Relation of higher folate intake to lower risk of Alzheimer disease in the elderly". Arch. Neurol. 64 (1): 86–92. doi:10.1001/archneur.64.1.86. PMID 17210813.
  24. ↑ Vitamins only of secondary benefit:
    • Morris MC, Evans DA, Schneider JA, Tangney CC, Bienias JL, Aggarwal NT (2006). "Dietary folate and vitamins B-12 and B-6 not associated with incident Alzheimer's disease". J. Alzheimers Dis. 9 (4): 435–43. PMID 16917153.
    • Malouf M, Grimley EJ, Areosa SA (2003). "Folic acid with or without vitamin B12 for cognition and dementia". Cochrane Database Syst Rev (4): CD004514. doi:10.1002/14651858.CD004514. PMID 14584018.
    • Sun Y, Lu CJ, Chien KL, Chen ST, Chen RC (2007). "Efficacy of multivitamin supplementation containing vitamins B6 and B12 and folic acid as adjunctive treatment with a cholinesterase inhibitor in Alzheimer's disease: a 26-week, randomised, double-blind, placebo-controlled study in Taiwanese patients". Clin Ther. 29 (10): 2204–14. doi:10.1016/j.clinthera.2007.10.012. PMID 18042476.
    • Boothby LA, Doering PL (2005). "Vitamin C and vitamin E for Alzheimer's disease". Ann Pharmacother. 39 (12): 2073–80. doi:10.1345/aph.1E495. PMID 16227450.
    • Gray SL, Anderson ML, Crane PK, Breitner JC, McCormick W, Bowen JD, Teri L, Larson E (2008). "Antioxidant vitamin supplement use and risk of dementia or Alzheimer's disease in older adults". J Am Geriatr Soc. 56 (2): 291–295. doi:10.1111/j.1532-5415.2007.01531.x. PMID 18047492.
  25. ↑ Curcumin in diet:
    • Garcia-Alloza M, Borrelli LA, Rozkalne A, Hyman BT, Bacskai BJ (2007). "Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model". Journal of Neurochemistry. 102 (4): 1095–1104. doi:10.1111/j.1471-4159.2007.04613.x. PMID 17472706.
    • Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM (2001). "The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse". Journal of Neuroscience. 21 (21): 8370–8377. PMID 11606625.
  26. ↑ Rosendorff C, Beeri MS, Silverman JM (2007). "Cardiovascular risk factors for Alzheimer's disease". Am J Geriatr Cardiol. 16 (3): 143–9. doi:10.1111/j.1076-7460.2007.06696.x. PMID 17483665.
  27. ↑ Gustafson D, Rothenberg E, Blennow K, Steen B, Skoog I (2003). "An 18-year follow-up of overweight and risk of Alzheimer disease". Arch. Intern. Med. 163 (13): 1524–1528. doi:10.1001/archinte.163.13.1524. PMID 12860573.
  28. ↑ Reiss AB, Wirkowski E (2007). "Role of HMG-CoA reductase inhibitors in neurological disorders : progress to date". Drugs. 67 (15): 2111–2120. PMID 17927279.
  29. ↑ Kuller LH (2007). "Statins and dementia". Current Atherosclerosis Reports. 9 (2): 154–161. doi:10.1007/s11883-007-0012-9. PMID 17877925.
  30. ↑ Szekely CA, Breitner JC, Fitzpatrick AL, Rea TD, Psaty BM, Kuller LH, Zandi PP (2008). "NSAID use and dementia risk in the Cardiovascular Health Study: role of APOE and NSAID type". Neurology. 70 (1): 17–24. doi:10.1212/01.wnl.0000284596.95156.48. PMID 18003940.
  31. ↑ "Long-term use of ibuprofen may reduce the risk of developing Alzheimer's disease, a large US study reports". BBC. 2008-05-05.
  32. ↑ "Ibuprofen Linked to Reduced Alzheimer's Risk". Washington Post. 2008-05-05.
  33. ↑ Craig MC, Murphy DG (2007). "Estrogen: effects on normal brain function and neuropsychiatric disorders". Climacteric. 10 Suppl 2: 97–104. doi:10.1080/13697130701598746. PMID 17882683.
  34. ↑ Mori K, Takeda M (2007). "Hormone replacement Up-to-date. Hormone replacement therapy and brain function". Clin Calcium (in Japanese). 17 (9): 1349–1354. doi:CliCa070913491354 Check |doi= value (help). PMID 17767023.
  35. ↑ Birks J, Grimley Evans J (2007). "Ginkgo biloba for cognitive impairment and dementia". Cochrane Database Syst Rev (2): CD003120. doi:10.1002/14651858.CD003120.pub2. PMID 17443523. Retrieved 2008-02-22.
  36. ↑ Verghese J, Lipton R, Katz M, Hall C, Derby C, Kuslansky G, Ambrose A, Sliwinski M, Buschke H (2003). "Leisure activities and the risk of dementia in the elderly". N Engl J Med. 348 (25): 2508–2516. doi:10.1056/NEJMoa022252. PMID 12815136.
  37. ↑ Bennett DA, Schneider JA, Tang Y, Arnold SE, Wilson RS (2006). "The effect of social networks on the relation between Alzheimer's disease pathology and level of cognitive function in old people: a longitudinal cohort study". Lancet Neurol. 5 (5): 406–412. doi:10.1016/S1474-4422(06)70417-3. PMID 16632311.
  38. ↑ Bialystok E, Craik FIM, Freedman M (2007). "Bilingualism as a protection against the onset of symptoms of dementia". Neuropsychologia. 42 (2): 459–464. doi:10.1016/j.neuropsychologia.2006.10.009.
  39. ↑ 39.0 39.1 39.2 39.3 "Practice Guideline for the Treatment of Patients with Alzheimer's disease and Other Dementias" (PDF). American Psychiatric Association. October 2007. doi:10.1176/appi.books.9780890423967.152139. Retrieved 2007-12-28.
  40. ↑ Bottino CM, Carvalho IA, Alvarez AM; et al. (2005). "Cognitive rehabilitation combined with drug treatment in Alzheimer's disease patients: a pilot study". Clin Rehabil. 19 (8): 861–869. doi:10.1191/0269215505cr911oa. PMID 16323385.
  41. ↑ Doody RS, Stevens JC, Beck C; et al. (2001). "Practice parameter: management of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology". Neurology. 56 (9): 1154–1166. PMID 11342679.
  42. ↑ Hermans DG, Htay UH, McShane R (2007). "Non-pharmacological interventions for wandering of people with dementia in the domestic setting". Cochrane Database Syst Rev (1): CD005994. doi:10.1002/14651858.CD005994.pub2. PMID 17253573.
  43. ↑ Robinson L, Hutchings D, Dickinson HO; et al. (2007). "Effectiveness and acceptability of non-pharmacological interventions to reduce wandering in dementia: a systematic review". Int J Geriatr Psychiatry. 22 (1): 9–22. doi:10.1002/gps.1643. PMID 17096455.
  44. ↑ Woods B, Spector A, Jones C, Orrell M, Davies S (2005). "Reminiscence therapy for dementia". Cochrane Database Syst Rev (2): CD001120. doi:10.1002/14651858.CD001120.pub2. PMID 15846613.
  45. ↑ Peak JS, Cheston RI (2002). "Using simulated presence therapy with people with dementia". Aging Ment Health. 6 (1): 77–81. doi:10.1080/13607860120101095. PMID 11827626.
  46. ↑ Camberg L, Woods P, Ooi WL; et al. (1999). "Evaluation of Simulated Presence: a personalised approach to enhance well-being in persons with Alzheimer's disease". J Am Geriatr Soc. 47 (4): 446–452. PMID 10203120.
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  58. ↑ Vaccination:
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