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Alzheimer's Disease in Wikipedia

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This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Alzheimer's disease". (Source - Retrieved 2006-09-07 14:10:33 from


Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive deterioration together with declining activities of daily living and neuropsychiatric symptoms or behavioral changes. It is the most common cause of dementia.

The most striking early symptom is short term memory loss (amnesia), which usually manifests as minor forgetfulness that becomes steadily more pronounced with illness progression, with relative preservation of older memories. As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language (aphasia), skilled movements (apraxia), recognition (agnosia), and those functions (such as decision-making and planning) closely related to the frontal and temporal lobes of the brain as they become disconnected from the limbic system, reflecting extension of the underlying pathological process.

This pathological process consists principally of neuronal loss or atrophy, principally in the temporoparietal cortex, but also in the frontal cortex, together with an inflammatory response to the deposition of amyloid plaques and neurofibrillary tangles.

The ultimate cause of the disease is unknown. Genetic factors are known to be important, and autosomal dominant mutations in three different genes (presenilin 1, presenilin 2, and amyloid precursor protein) have been identified that account for a small number of cases of familial, early-onset AD. For late onset AD (LOAD), only one susceptibility gene has so far been identified: the epsilon 4 allele of the apolipoprotein E gene. Age of onset itself has a heritability of around 50%.


Alois Alzheimer
Emil Kraepelin

The symptoms of the disease as a distinct entity were first identified by Emil Kraepelin. The characteristic neuropathology was first observed by Alois Alzheimer, a German psychiatrist, after whom the disease is named, in 1906. In this sense, the disease was co-discovered by Kraepelin and Alzheimer, who worked in Kraepelin's laboratory. Because of the overwhelming importance Kraepelin attached to finding the neuropathological basis of psychiatric disorders, Kraepelin made the generous decision that the disease would bear Alzheimer's name. [1]

For most of the twentieth century, the diagnosis of Alzheimer's disease was reserved for individuals between the ages of 45-65 who developed symptoms of presenile dementia due to the histopathologic process discovered by Dr. Alzheimer (see below for description of brain tissue changes). During this time senile dementia itself (as a set of symptoms) was considered to be a more or less normal outcome of the aging process, and thought to be due to age-related brain arterial "hardening." In the 1970s and early 1980s, because the symptoms and brain pathology were identical for Alzheimer victims older and younger than age 65, the name "Alzheimer's disease" began to be used, within and outside the medical profession, equally for afflicted individuals of all ages, although in this period the term senile dementia of the Alzheimer type (SDAT) was often used to distinguish those over 65 who did not fit the classical age criterion. Eventually, the term Alzheimer's disease was adopted formally in the psychiatric and neurological nomenclature to describe individuals of all ages with the characteristic common symptom pattern, disease course, and neuropathology. The term Alzheimer disease (without the apostrophe and s) also continues to be used commonly in the literature.

Clinical features

The usual first symptom noticed is short term memory loss which progresses from seemingly simple and often fluctuating forgetfulness (with which the disease should not be confused) to a more pervasive loss of short-term memory, then of familiar and well-known skills or objects or persons. Aphasia, disorientation and disinhibition often accompany the loss of memory. Alzheimer's disease may also include behavioral changes, such as outbursts of violence or excessive passivity in people who have no previous history of such behavior. In the later stages, deterioration of musculature and mobility, leading to bedfastness, inability to feed oneself, and incontinence, will be seen if death from some external cause (e.g. heart attack or pneumonia) does not intervene. Average duration of the disease is approximately 7-10 years, although cases are known where reaching the final stage occurs within 4-5 years, or up to 15 years.

Stages & Symptoms

  • Mild - At the early stage of the disease, patients have a tendency to become less energetic or spontaneous, though changes in their behaviour often goes unnoticed even by the patients' immediate family.
  • Moderate - As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities.
  • Severe - As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need to be supervised with everything they are doing.


The diagnosis is made primarily on the basis of history, clinical observation and tests of memory and intellectual functioning over a series of weeks or months, with various physical tests (blood tests and neuroimaging) being performed to rule out alternative diagnoses. No medical tests are available to diagnose Alzheimer's disease conclusively pre-mortem. Expert clinicians who specialize in memory disorders can now diagnose AD with an accuracy of 85-90%, but a definitive diagnosis of Alzheimer's disease must await microscopic examination of brain tissue, generally at autopsy. Functional neuroimaging studies such as PET and SPECT scans can provide a supporting role where dementia is clearly present, but the type of dementia is questioned. Recent studies suggest that SPECT neuroimaging approaches clinical exam in diagnostic accuracy and may outperform exam at differentiating types of dementia (Alzheimer's disease vs. vascular dementia). [2][3] However, Alzheimer's disease remains a primarily clinical diagnosis based on the presence of characteristic neurological features and the absence of alternative diagnoses, with neuroimaging providing a supporting role where dementia is clearly present, but the type of dementia is questioned.

Interviews with family members and/or caregivers are extremely important in the initial assessment, as the sufferer him/herself may tend to minimize his symptomatology or may undergo evaluation at a time when his/her symptoms are less apparent, as quotidian fluctuations ("good days and bad days") are a fairly common feature. Such interviews also provide important information on the affected individual's functional abilities, which are a key indicator of the significance of the symptoms and the stage of dementia.

Initial suspicion of dementia may be strengthened by performing the mini mental state examination, after excluding clinical depression. Psychological testing generally focuses on memory, attention, abstract thinking, the ability to name objects, visuospatial abilities, and other cognitive functions. Results of psychological tests may not readily distinguish Alzheimer's disease from other types of dementia, but can be helpful in establishing the presence of and severity of dementia. They can also be useful in distinguishing true dementia from temporary (and more treatable) cognitive impairment due to depression or psychosis, which has sometimes been termed "pseudodementia".



There are several characteristic neuropathological changes found in the brain in AD:

  • The deposition of an abnormal protein (amyloid beta) outside nerve cells in the form of amyloid. These are called diffuse plaques and amyloid also forms the core of more organized plaques called senile or neuritic plaques. Recently evidence has begun to accumulate implicating simpler, soluble forms of amyloid (oligomers) in the pathological process, and the presence of plaque amyloid does not correlate well with the degree of dementia. Amyloid also accumulates in the walls of small blood vessels in the brain. This is termed amyloid angiopathy (also called congophilic angiopathy).
  • Accumulation of abnormal protein filaments inside nerve cells in the brain, formed from aggregation of tau protein, which normally stabilizes microtubules. In AD, an abnormally phosphorylated form of tau protein accumulates as paired helical filaments. Tau accumulates in various forms:
    MRI images of Alzheimer's and normal brains
    • As masses of filaments inside nerve cell body termed neurofibrillary tangles
    • Inside nerve cell processes in the brain termed neuropil threads
    • Inside nerve cell processes that surround amyloid plaques - termed dystrophic neurites or plaque neurites.
  • Diffuse atrophy and loss of neurons, neuronal processes and synapses in the cerebral cortex and certain subcortical regions. This results in gross atrophy of the affected regions and enlargement of the lateral ventricles.


Levels of the neurotransmitter acetylcholine are reduced. Levels of the neurotransmitters serotonin, norepinephrine, and somatostatin are also often reduced. Glutamate levels are usually elevated.

Disease mechanism

Three major competing hypotheses exist to explain the cause of the disease.

The oldest hypothesis is the "cholinergic hypothesis". It states that Alzheimer's begins as a deficiency in the production of acetylcholine, a vital neurotransmitter. Much early therapeutic research was based on this hypothesis, including restoration of the "cholinergic nuclei". The possibility of cell-replacement therapy was investigated on the basis of this hypothesis. All of the first-generation anti-Alzheimer's medications are based on this hypothesis and work to preserve acetylcholine by inhibiting acetylcholinesterases (enzymes that break down acetylcholine). These medications, though sometimes beneficial, have not led to a cure. In all cases, they have served to only treat symptoms of the disease and have neither halted nor reversed it. These results and other research have led to the conclusion that acetylcholine deficiencies may not be directly causal, but are a result of widespread brain tissue damage, damage so widespread that cell-replacement therapies are likely to be impractical.

The other two hypotheses each have their advocates, and have often been described (lightheartedly) as the "tau-ist" and "ba-ptist" viewpoints in scientific publications by Alzheimer's disease researchers. "Tau-ists" believe that the tau protein abnormalities come first and lead to a full disease cascade. "Ba-ptists" believe that beta amyloid deposits are the causative factor in the disease. For example, the presence of the APP gene on chromosome 21 is believed to explain the high incidence of early-onset AD pathology in patients with Down syndrome, who carry three copies of chromosome 21 and thus APP itself. The "ba-ptist" theory is finding new supporters due to recent discoveries of impaired vascular and cerebrospinal fluid transport of beta amyloid out of the brain tissues, resulting in a greater risk for plaque formation. A third protein, alpha-synuclein, which has already been shown to be important in Parkinson's disease, has also been demonstrated to be associated with amyloid plaques in AD. This hypothesis has been given the name "syn-ners" among AD researchers. There is also a "triple lesion" hypothesis that proposes a pathological interaction among these three candidate proteins. The extent of each protein's contribution may determine whether or not the "lesion disorder" manifests as AD, Parkinsonism, or other degenerative diseases.

Abnormal protein aggregation in the brain is a common thread in neurodegenerative disorders. Besides beta-amyloid in Alzheimer's and synuclein in Parkinson's, examples include prions in prion diseases; huntingtin in Huntington's disease; BRI in familial British dementia; and tau protein in frontotemporal dementia with Parkinson's disease, progressive supernuclear palsy, and Pick's disease. See also: Lewy body. Many reaserchers believe the protein aggregates formed are toxic and give rise to the multiple brain changes that characterize the different neurodegenerative diseases. If one relationship between these diseases really is abnormal protein aggregation, then discovering ways to prevent aggregation, or the processes set in motion by the aggregation, may halt the disease process. The presence of plaques and tangles, however, does not always correlate well with clinical Alzheimer's; in other words, not all people who have plaques and/or tangles manifest symptoms of the disease. Loss of synapses correlates much better with the decline of cognition than the presence of plaques and tangles, as well as loss of dendrites and dendritic spines. Some recent research is focusing on the possibility that plaques and tangles arise as a defense against another, as yet undiscovered, process or substance that itself causes the disease. Researchers are intrigued by the idea that the plaques and tangles might not be the problem, but rather a symptom of the problem. The plaques and neurofibrillary tangles may be the result of the brains's efforts to contain the abnormal proteins produced by the disease.

Genetics of AD

Rare cases are caused by dominant genes that run in families. These cases often have an early age of onset. Mutations in presenilin-1 or presenilin-2 genes have been documented in some families. Mutations of presenilin 1 (PS1) lead to the most aggressive form of familial AD (FAD). Evidence from rodent studies suggests that the FAD mutation of PS1 results in impaired hippocampal-dependent learning which is correlated with reduced adult neurogenesis in the dentate gyrus [7]). Mutations in the APP gene on chromosome 21 can also cause early onset disease. The presenilins have been identified as essential components of the proteolytic processing machinery that produces beta amyloid peptides through cleavage of APP.

Unfortunately, the most obviously genetic cases are also the rarest. Most cases identified are "sporadic" with no clear family history. It is probable that environmental factors have to interact with a genetic susceptibility to cause development of disease. Head injury has been consistently shown to be linked to later development of AD in epidemiological studies. In addition, small cranial diameter has been shown to correlate well with early onset of recognizable symptoms. Inheritance of the epsilon 4 allele of the ApoE gene is regarded as a risk factor for development of disease, but large-scale genetic association studies raise the possibility that even this does not indicate susceptibility so much as how early one is likely to develop Alzheimer's. There is speculation among genetic experts that there are other risk and protective factor genes that may influence the development of late onset Alzheimer's disease (LOAD). Intriguing work is currently going on investigating the possibility that the regulatory regions of various Alzheimer's associated genes could be important in sporadic Alzheimer's, especially inflammatory activation of these genes. These hypotheses include the amyloid beta precursor protein [8], the beta secretase enzymes [9], insulin-degrading enzyme [10], endothelin-converting enzymes [11], and inflammatory 5-lipoxygenase gene [12].

Genetic linkage

Alzheimer's disease is definitely linked to the 1st, 14th, and 21st chromosomes, but other linkages are controversial and not, as yet, confirmed. While some genes predisposing to AD have been identified , such as ApoE4 on chromosome 19, sporadic AD also involves other risk and protective genes still awaiting confirmation.

Epidemiology and prevention

Alzheimer's disease is the most frequent type of dementia in the elderly and affects almost half of all patients with dementia. Correspondingly, advancing age is the primary risk factor for Alzheimer's. Among people aged 65, 2-3% show signs of the disease, while 25 - 50% of people aged 85 have symptoms of Alzheimer's and an even greater number have some of the pathological hallmarks of the disease without the characteristic symptoms. Every five years after the age of 65, the probability of having the disease doubles. The proportion of people with Alzheimer's begins to decrease after age 85 because of the increased mortality due to the disease, and relatively few people over the age of 100 have the disease.

The evidence relating certain behaviors, dietary intakes, environmental exposures, and diseases to the likelihood of developing Alzhemier's varies in quality and its acceptance by the medical community. It is important to understand that interventions that reduce the risk of developing disease in the first place may not alter disease progression after symptoms become apparent. Due to their observational design, studies examining disease risk factors are often at risk from confounding variables. Several recent large, randomized controlled trials—in particular the Women's Health Initiative—have called into question preventive mesasures based on cross-sectional studies. Some proposed preventive measures are even based on studies conducted solely in animals.

Risk reducers

  • Intellectual stimulation (e.g., playing chess or doing the crossword) [4]
  • Regular physical exercise [5]
  • Regular social interaction
  • A generally healthy diet low in saturated fat, supplemented in particular with:
  • Cholesterol-lowering drugs (statins) reduce Alzheimer's risk in observational studies but so far not in randomized controlled trials
  • Hormone replacement therapy is no longer thought to prevent dementia based on data from the Women's Health Initiative
  • Regular use of non-steroidal anti-inflammatory drugs like ibuprofen and aspirin reduces the chance of dementia but the risks appear to outweigh the drugs' benefit as a method of primary prevention

Risk factors


There is currently no cure for Alzheimer's disease, although there are drugs which offer symptomatic benefit, specifically with respect to short-term memory impairment. In 2006, the American Association for Geriatric Psychiatry published a position paper with treatment guidelines for patients with Alzheimer’s disease. [18]

Acetylcholinesterase inhibitors

Acetylcholinesterase (AChE) inhibition was thought to be important because there is a reduction in activity of the cholinergic neurons. AChE-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons). Acetylcholinesterase-inhibitors seemed to modestly moderate symptoms but do not prevent disease progression including cell death.

Examples include:

  • tacrine - no longer clinically used
  • donepezil - (marketed as Aricept)
  • galantamine - (marketed as Razadyne, formerly Reminyl)
  • rivastigmine - (marketed as Exelon)

Recently, a controversy has erupted about cholinesterase inhibitors because a study in the respected medical journal The Lancet has suggested they are ineffective.[19] The pharmaceutical companies, but also many independent clinicians, dispute the findings of the study, based on methodologic grounds. A transdermal patch is under development that may ease administration of rivastigmine.[20]

NMDA antagonists

Recent evidence of the involvement of glutamatergic neuronal excitotoxicity in the aetiology of Alzheimer's disease led to the development and introduction of memantine. Memantine is a novel NMDA receptor antagonist, and has been shown to be moderately clinically efficacious. [21]

Potential treatments

A large number of potential treatments for Alzheimer's disease are currently under investigation, including four compounds being studied in phase 3 clinical trials. Xaliproden had been shown to reduce neurodegeneration in animal studies. [22] Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques. R-flurbiprofen (MPC-7869) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide. [23] [24] Leuprolide is also being studied for Alzheimer’s. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages. [25]

  • Vaccines for Alzheimer's, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention. Ongoing efforts are based on the idea that, by training the immune system to recognize and attack beta-amyloid, the immune system might reverse deposition of amyloid and thus stop the disease. Initial results using this approach in animals were promising. However, when the first vaccines were used in humans, a small fraction of participants (6%, 18 of 300) developed encephalitis and the trials were stopped. Participants in the halted trials continued to be followed, and some showed possible benefit in the form of slower progression of the disease. [26] Work is continuing on less toxic Aβ vaccines, such as a DNA-based therapy that recently showed promise in mice.
  • Proposed alternative treatments for Alzheimer's include a range of herbal compounds and dietary supplements. In general, research on the efficacy of these substances is either non-existent or far too weak to support therapeutic claims of improved memory or slowed disease progression.

In a 2006 review by the American Association for Geriatric Psychiatry (AAGP) [27] vitamin E in doses below 400 IU was mentioned as having conflicting evidence in efficacy to prevent AD. Higher doses were discouraged as these may be linked with higher mortality. Ginko biloba did not show enough long-term efficacy for the Task force to recommend its use, but it is being studied in a large randomized clinical study. [28]

Laboratory studies with cells and animals continually fuel the pipeline of potential treatments. Some currently approved drugs such as statins and thiazolidinediones [29] have also been under investigation for the treatment and prevention of Alzheimer’s. Recent clinical trials for Phase 2 and Phase 3 in this category have taken 12 to 18 months under study drug, plus addtional months for patient enrollment and analysis. Compounds that are just entering into human trials or are in pre-clinical trials would be at least 4 years from being available to the public and would be available only if they can demonstrate safety and efficacy in human trials.

Social issues

Alzheimer's is considered to be a major public health challenge since the median age of the industrialized world's population is increasing gradually. Indeed, 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. The role of family caregivers has also become more prominent, as 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.

Caregivers (called "carers" in Europe) often give up time from work and forego pay to care for someone. Alzheimer's has a high cost of care, with nearly \$77,500 in unpaid and paid care for an Alzheimer's patient over the course of one year in the US. Informal care takes up about 47 hours per week for Alzheimer's caregivers and more than 70% of caregiver respondants to a 2006 survey said they could not leave their loved one alone. [30]

Famous Alzheimer's disease sufferers have included President Ronald Reagan, Charlton Heston, Ralph Waldo Emerson, and Rita Hayworth.

See also


  1. ^ Kraepelin, E. J. Psychiat. Res., 1997, Vol 31, No. 6, pp. 635-643
  2. ^ Dougall NJ, Bruggink S, Ebmeier KP. (2004) Systematic review of the diagnostic accuracy of 99mTc-HMPAO-SPECT in dementia. Am J Geriatr Psychiatry 12: 554-70. PMID 15545324.
  3. ^ Bonte FJ, Harris TS, Hynan LS, Bigio EH, White CL 3rd. (2006) Tc-99m HMPAO SPECT in the differential diagnosis of the dementias with histopathologic confirmation. Clin Nucl Med. 31:376-8. PMID 16785801
  4. ^ Verghese, Joe, Lipton, Richard B., Katz, Mindy J., Hall, Charles B., Derby, Carol A., Kuslansky, Gail, Ambrose, Anne F., Sliwinski, Martin, Buschke, Herman. Leisure Activities and the Risk of Dementia in the Elderly. N Engl J Med 2003 348: 2508-2516 [1]
  5. ^ Larson EB, Wang L, Bowen JD, McCormick WC, Teri L, Crane P, Kukull W. Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older. Ann Intern Med. 2006 Jan 17;144(2):73-81 PMID 16418406
  6. ^ Lim WS, Gammack JK, Van Niekerk JK, Dangour AD. Omega 3 fatty acid for the prevention of dementia. The Cochrane Database of Systematic Reviews 2006, Issue 1. PMID 16437528
  7. ^ Morris MC, Evans DA, Tangney CC, Bienias JL, Wilson RS. Fish consumption and cognitive decline with age in a large community study. Arch Neurol. 2005 Dec;62(12):1849-53 PMID 16216930
  8. ^ Lau FC, Shukitt-Hale B, Joseph JA. The beneficial effects of fruit polyphenols on brain aging. Neurobiol Aging. 2005 Dec;26 Suppl 1:128-32. Epub 2005 Sep 27. PMID 16194581.
  9. ^ Ramirez MR, Izquierdo I, do Carmo Bassols Raseira M, Zuanazzi JA, Barros D, Henriques AT. Effect of lyophilised Vaccinium berries on memory, anxiety and locomotion in adult rats. Pharmacol Res. 2005 Dec;52(6):457-62. Epub 2005 Aug 10. PMID 16098760.
  10. ^ Joseph JA, Denisova NA, Arendash G, Gordon M, Diamond D, Shukitt-Hale B, Morgan D. Blueberry supplementation enhances signaling and prevents behavioral deficits in an Alzheimer disease model. Nutr Neurosci. 2003 Jun;6(3):153-62. PMID 12793519.
  11. ^ Dai Q, Borenstein AR, Wu Y, Jackson JC, Larson EB. Fruit and vegetable juices and Alzheimer's disease: the Kame Project. Am J Med. 2006 Sep;119(9):751-9 PMID 16945610.
  12. ^ Joseph JA, Fisher DR, Carey.Fruit extracts antagonize Abeta- or DA-induced deficits in Ca2+ flux in M1-transfected COS-7 cells. J Alzheimers Dis. 2004 Aug;6(4):403-11; discussion 443-9. PMID 15345811.
  13. ^ Ng TP, Chiam PC, Lee T, Chua HC, Lim L, Kua EH. Curry Consumption and Cognitive Function in the Elderly. Am J Epidemiol. 2006 Jul 26. PMID 16870699.
  14. ^ Petersen RC, Thomas RG, Grundman M, Bennett D, Doody R, Ferris S, Galasko D, Jin S, Kaye J, Levey A, Pfeiffer E, Sano M, van Dyck CH, Thal LJ; Alzheimer's Disease Cooperative Study Group. "Vitamin E and donepezil for the treatment of mild cognitive impairment." N Engl J Med 352:2379-2388. PMID 15829527
  15. ^ Zandi PP, Anthony JC, Khachaturian AS, Stone SV, Gustafson D, Tschanz JT, Norton MC, Welsh-Bohmer KA, Breitner JC; Cache County Study Group. "Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study." Arch Neurol. 2004 61:82-88. PMID 14732624
  16. ^ [2]
  17. ^ Squitti R. et al. (2006) "Excess of nonceruloplasmin serum copper in AD correlates with MMSE, CSF beta-amyloid, and h-tau." Neurology 67-76-82. PMID 16832081
  18. ^ Constantine G. Lyketsos, Christopher C. Colenda, Cornelia Beck, Karen Blank, Murali P. Doraiswamy, Douglas A. Kalunian, Kristine Yaffe Position Statement of the American Association for Geriatric Psychiatry Regarding Principles of Care for Patients With Dementia Resulting From Alzheimer Disease. Am. J. Geriatr. Psychiatry 2006 14: 561-573 PMID: 16816009 [3]
  19. ^ Courtney C, Farrell D, Gray R, Hills R, Lynch L, Sellwood E, Edwards S, Hardyman W, Raftery J, Crome P, Lendon C, Shaw H, Bentham P; AD2000 Collaborative Group. Long-term donepezil treatment in 565 patients with Alzheimer's disease (AD2000): randomised double-blind trial. Lancet 2004;363:2105-15. PMID 15220031
  20. ^ Exelon Patch, The First Transdermal Therapy For Alzheimer's Disease, May Provide Promising New Approach To Treatment Of Dementia
  21. ^ Areosa SA, McShane R, Sherriff F. Memantine for dementia. Cochrane Database Syst Rev 2004(4). PMID 15495043
  22. ^ Lemaire L, et al, “Magnetic resonance imaging of the neuroprotective effect of xaliproden in rats” Invest Radiol. 2002 Jun;37(6):321-7. PMID 12021588
  23. ^ Zamrini, E. Geriatrics Aging. “Emerging Drug Therapies for Dementia” 2006;9(2):107,110-113. [4]
  24. ^ Eriksen JL, et al. "NSAIDs and enantiomers of flurbiprofen target gamma-secretase and lower Abeta 42 in vivo" J Clin Invest. 2003 Aug;112(3):440-9 PMID 12897211
  25. ^ Casadesus G, Garrett MR, et al. “The estrogen myth: potential use of gonadotropin-releasing hormone agonists for the treatment of Alzheimer's disease” Drugs R D. 2006;7(3):187-93. PMID 16752944
  26. ^
  27. ^ Lyketsos CG, Colenda CC, Beck C, Blank K, Doraiswamy MP, Kalunian DA, affe K; Task Force of American Association for Geriatric Psychiatry. “Position statement of the American Association for Geriatric Psychiatry regarding principles of care for patients with dementia resulting from Alzheimer disease” Am J Geriatr Psychiatry. 2006 Jul;14(7):561-72. PMID 16816009 [5]
  28. ^ Birks J, Grimley Evans J. "Ginkgo Biloba for cognitive impairment and dementia." Cochrane Database Syst Rev 2002(4). PMID 12519586
  29. ^ Landreth G. “PPARgamma agonists as new therapeutic agents for the treatment of Alzheimer's disease.” Exp Neurol. 2006 Jun;199(2):245-8. PMID 16733054
  30. ^ MetLife Mature Market Institute, The MetLife Study of Alzheimer’s Disease: The Caregiving Experience, August 2006 [6]

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