Prevalence Of Alzheimer's Disease Research Articles

Lithium may be useful in the prevention of Alzheimer’s disease in individuals at risk of presenile familial Alzheimer’s disease

Alzheimer's disease (AD) is the most common form of dementia among older people. Presenile familial AD (FAD) and sporadic Alzheimer's disease (SAD) have identical brain lesions, containing senile plaques with beta-amyloid (Abeta) peptide and neurofibrillary tangles formed by hyperphosphorylation of a microtubule-associated protein known as tau. However, FAD and SAD differ in onset and genetic transmission. Unlike SAD, presenile FAD is transmitted as a pure autosomal dominant trait. The authors suggest that lithium could be used for AD prevention, particularly in individuals at risk of presenile FAD, which has early onset. Evidence supporting this hypothesis suggests that lithium decreases Abeta peptide production and inhibits the activity of glycogen synthase kinase-3 which induces aggregation of tau protein into tangles, and tau hyperphosphorylation. Prevalence of AD is lower in patients with chronic lithium treatment, which also increases brain-derived neurotrophic factor activity, so might prevent onset in patients at risk for AD. Several considerations are suggested for prevention trials: the effect of lithium could be evaluated in young animal models that express presenile FAD mutant genes; the time, dose, duration and monitoring of lithium therapy are considered; early phenotypes could be monitored for treatment effect; and some other agents, like valproic acid, could also be candidates for prevention.

Impaired Adult Neurogenesis in the Dentate Gyrus of a Triple Transgenic Mouse Model of Alzheimer's Disease

It has become generally accepted that new neurones are added and integrated mainly in two areas of the mammalian CNS, the subventricular zone and the subgranular zone (SGZ) of the dentate gyrus (DG) of the hippocampus, which is of central importance in learning and memory. The newly generated cells display neuronal morphology, are able to generate action potentials and receive functional synaptic inputs, i.e. their properties are similar to those found in mature neurones. Alzheimer's disease (AD) is the primary and widespread cause of dementia and is an age-related, progressive and irreversible neurodegenerative disease that deteriorates cognitive functions. Here, we have used male and female triple transgenic mice (3xTg-AD) harbouring three mutant genes (β-amyloid precursor protein, presenilin-1 and tau) and their respective non-transgenic (non-Tg) controls at 2, 3, 4, 6, 9 and 12 months of age to establish the link between AD and neurogenesis. Using immunohistochemistry we determined the area density of proliferating cells within the SGZ of the DG, measured by the presence of phosphorylated Histone H3 (HH3), and their possible co-localisation with GFAP to exclude a glial phenotype. Less than 1% of the HH3 labeled cells co-localised with GFAP. Both non-Tg and 3xTg-AD showed an age-dependent decrease in neurogenesis. However, male 3xTg-AD mice demonstrated a further reduction in the production of new neurones from 9 months of age (73% decrease) and a complete depletion at 12 months, when compared to controls. In addition, female 3xTg-AD mice showed an earlier but equivalent decrease in neurogenesis at 4 months (reduction of 63%) with an almost inexistent rate at 12 months (88% decrease) compared to controls. This reduction in neurogenesis was directly associated with the presence of β-amyloid plaques and an increase in the number of β-amyloid containing neurones in the hippocampus; which in the case of 3xgTg females was directly correlated. These results suggest that 3xTg-AD mice have an impaired ability to generate new neurones in the DG of the hippocampus, the severity of which increases with age and might be directly associated with the known cognitive impairment observed from 6 months of age onwards . The earlier reduction of neurogenesis in females, from 4 months, is in agreement with the higher prevalence of AD in women than in men. Thus it is conceivable to speculate that a recovery in neurogenesis rates in AD could help to rescue cognitive impairment.

S4-03-05: Insulin resistance/metabolic syndrome and cognitive impairment

With the aging of the US population, the incidence and prevalence of Alzheimer disease (AD) and other forms of dementia are expected to quadruple over the next 50 years. The projected exponential expansion of the population affected by dementia, along with its downstream effects on society, highlight the imperative for developing effective treatment and preventative strategies. An exciting new body of literature has highlighted how metabolic dysregulation in the setting of diabetes, insulin resistance and obesity may trigger accelerated cognitive aging. We will review state-of-the-art science related to metabolic syndrome and insulin resistance and risk of dementia and propose future directions for this emerging and highly significant field. Metabolic syndrome and insulin resistance represent important risk factors for the development of cognitive impairment and may offer strategies for novel treatment and preventative strategies.

P4-076: Dietary patterns during early adult life associated with Alzheimer's disease: A population based-study (BERCAL)

Dietary pattern analysis has emerged as a possible approach to examining diet-disease relations in Alzheimer's disease (AD). In contrast with the conventional approach, which focuses on a single nutrient or a few nutrients or foods, this approach considers overall eating patterns. We examined the dietary patterns determined by factor analysis of dietary data collected with a food-frequency questionnaire in people with Alzheimer's disease and healthy controls. Diet data were obtained as part of a population based study of the prevalence of AD in Poland (Lublin district – 2 million inhabitants). Stratified sampling and random selection strategies were combined to obtain a representative population for screening (ages >55 in a sample of 2100 persons). From the screened population, 71 persons were diagnosed with AD; the same number of healthy, age and gender matched (F/M 42/29) controls was selected. The two groups did not differ with respect to other chronic diseases. A food frequency questionnaire with 35 food groups representative of this population's diets was developed. Caregivers of AD patients and healthy controls were interviewed to obtain diet histories and food frequencies of foods consumed during early adult life. Factor analysis (principal component) was used to derive food patterns. The factors were rotated by an orthogonal transformation (Varimax rotation) to achieve simpler structure with greater interpretability. Factor scores for each pattern were then obtained for each subject using composite scores of variables that loaded highly on each factor. We identified two major eating patterns: 1) High carbohydrate and fat, and 2) Low fat and vegetables. The early adult life pattern for AD patients was characterized by greater intakes of cakes, potatoes, white breads, eggs, processed meats, sugar, pork and cheese. The patterns for healthy controls included greater intakes of soups, poultry, fish, dark breads, potatoes, vegetables and yogurt. Dietary patterns during early adult life may be a risk factor for AD. This small study indicates early life dietary patterns as defined by factor analysis with data from a food frequency questionnaire as characteristic for Alzheimer's disease in a population of Poland.

Alzheimer's Disease Prevalence can be Lowered with Non-Invasive Testing

Cardiovascular and cerebrovascular disease are reported to be major risk factors to Alzheimer's disease (AD). These risk factors mainly affect the elderly (over age 60) and previously were believed to only promote vascular dementia (VaD). Cardiovascular and cerebrovascular pathology involving structural lesions of the heart and carotid or vertebral artery stenosis stemming from intima media thickening or vessel plaque formation can insidiously reduce blood flow to the brain. Since heart and carotid artery disease are common findings in elderly patients and can provoke chronic cerebral hypoperfusion, we submit that individuals with even very mild memory complaints should undergo screening using echocardiography and carotid Doppler ultrasound. These non-invasive, safe, cost-effective ultrasound techniques can often detect correctable or treatable early lesions involving the carotid arteries and the heart that contribute to cerebral hypoperfusion. Inasmuch as cerebral hypoperfusion can be a pathophysiologic trigger of AD, its prevention or attenuation should tangibly reverse or at least delay the onset and impact of severe cognitive meltdown. This clinical approach may have an important impact in reducing the number of new AD and VaD cases and lessen the catastrophic socio-economic burden these dementias are expected to have on the US healthcare system in the near future.

Prevalence of Alzheimer's disease with diabetes in the Japanese population

AbstractBackground: The aim of the present study was to estimate the prevalence of impaired cognitive function and Alzheimer's disease (AD) in diabetic subjects from Japan.Methods: In the present study, 386 Japanese diabetic subjects aged more than 50 years were initially screened with the ‘brief screening test’ for AD, and were diagnosed with AD and vascular dementia (VaD) according to the criteria of the NINCDS‐ADRDA and the NINDS‐AIREN. We compared the prevalence of dementia in diabetic patients with that in ordinary subjects, and analyzed the association of the status of diabetes with dementia including AD and VaD.Results: Forty‐six (11.9%) patients were diagnosed with dementia, including 13 (3.4%) patients with AD and nine (2.3%) patients with VaD. Of the 221 subjects aged more than 65 years, 39 (17.6%) patients had dementia, including 13 (5.9%) patients with AD and eight (3.6%) patients with VaD. Compared with ordinary subjects, the prevalence of dementia in the present study was more frequent than the prevalence of dementia for the general population in almost each age group examined. There was also a greater prevalence of AD and VaD in subjects aged over 65 years in the present study. In the present study, AD subjects had significantly higher levels of fasting plasma glucose (FPG; 247.5 ± 116.3 mg/dL; P < 0.05) and glycosylated hemoglobin (HbA1c; 8.8 ± 1.9%; P < 0.01) compared with non‐demented subjects. In AD patients, the odds ratios of FPG and HbA1c were also significantly higher (1.02 and 2.07, respectively; both P < 0.01).Conclusion: The present study shows that diabetes can be associated with impaired cognitive function, particularly AD, in Japanese subjects.

Atrophy accelerates with conversion from mild cognitive impairment to Alzheimer disease

If the current rates of growth of the senior population and prevalence of Alzheimer disease (AD) continue, the number of individuals worldwide affected by this disabling disease will double from 24.3 to 42.3 million by 2020.1 Given the devastating impact of AD on patient, family, community, and society, considerable efforts are underway to unravel its pathophysiologic mechanisms, with the aim of developing safe and effective disease-modifying therapies. Such therapies will probably be most efficacious in the early symptomatic or ideally pre-symptomatic stages of the disease.2 An accurate diagnosis of AD in the early symptomatic stage is extremely challenging despite the development of useful clinical constructs like mild cognitive impairment (MCI), which enables the identification of individuals who may be in an early clinical phase of AD. Future diagnostic approaches toward early symptomatic and presymptomatic AD will almost certainly hinge upon biomarkers. In fact, new diagnostic criteria were recently proposed that operationalize the pre-dementia diagnosis of AD and include imaging and CSF biomarkers as supportive evidence.3 Beyond their use in diagnostics, imaging and other biomarkers will likely serve important roles in monitoring effects of …

Alzheimer’s disease: epidemiology, genetics, and beyond

Alzheimer's disease (AD) is an increasing epidemic threatening public health. Both men and women are susceptible to the disease although women are at a slightly higher risk. The prevalence of AD rises exponentially in elderly people from 1% at age of 65 to approximately 40%-50% by the age of 95. While the cause of the disease has not been fully understood, genetics plays a role in the onset of the disease. Mutations in three genes (APP, PSEN1, and PSEN2) have been found to cause AD and APOE4 allele increases the risk of the disease. As human genomic research progresses, more genes have been identified and linked with AD. Genetic screening tests for persons at high risk of AD are currently available and may help them as well as their families better prepare for a later life with AD.

Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set

Alzheimer's Disease (AD) is the most widespread form of dementia during the later stages of life. If improved therapeutics are not developed, the prevalence of AD will drastically increase in the coming years as the world's population ages. By identifying differences in neuronal gene expression profiles between healthy elderly persons and individuals diagnosed with AD, we may be able to better understand the molecular mechanisms that drive AD pathogenesis, including the formation of amyloid plaques and neurofibrillary tangles. In this study, we expression profiled histopathologically normal cortical neurons collected with laser capture microdissection (LCM) from six anatomically and functionally discrete postmortem brain regions in 34 AD-afflicted individuals, using Affymetrix Human Genome U133 Plus 2.0 microarrays. These regions include the entorhinal cortex, hippocampus, middle temporal gyrus, posterior cingulate cortex, superior frontal gyrus, and primary visual cortex. This study is predicated on previous parallel research on the postmortem brains of the same six regions in 14 healthy elderly individuals, for which LCM neurons were similarly processed for expression analysis. We identified significant regional differential expression in AD brains compared with control brains including expression changes of genes previously implicated in AD pathogenesis, particularly with regard to tangle and plaque formation. Pinpointing the expression of factors that may play a role in AD pathogenesis provides a foundation for future identification of new targets for improved AD therapeutics. We provide this carefully phenotyped, laser capture microdissected intraindividual brain region expression data set to the community as a public resource.

Gender differences in susceptibility to kainic acid-induced neurodegeneration in aged C57BL/6 mice

Some epidemiological studies concerning gender differences in Alzheimer's disease (AD) support the higher prevalence and incidence of AD in women, while most studies using animal models of aging have included only male subjects. It is still uncommon for aged males and females to be compared in the same study. In the present study, we investigated how age and gender influence the excitotoxic neurodegeneration by treating C57BL/6 mice (aged females and males as well as adult females and males) with kainic acid (KA) intranasally. Clinical signs, behavioural changes, pathological changes and astrocyte proliferation were tested; and the levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were measured after KA treatment. The results showed that aged female mice were more sensitive to KA-induced excitotoxicity as demonstrated by severer seizure activity, increased locomotion and rearing in open-field test, prominent hippocampal neuronal damage, enhanced astrocyte proliferation compared with aged males, adult females and adult male mice. In addition, higher BDNF level in hippocampus of aged female mice was observed. These results denote the disparity of aging and gender in KA-induced hippocampal neurodegeneration and aged female mice are more sensitive to the excitotoxicity.

Regional Analysis of Spontaneous MEG Rhythms in Patients with Alzheimer’s Disease Using Spectral Entropies

Alzheimer's disease (AD) is the most common form of dementia. Ageing is the greatest known risk factor for this disorder. Therefore, the prevalence of AD is expected to increase in western countries due to the rise in life expectancy. Nowadays, a low diagnosis accuracy is reached, but an early and accurate identification of AD should be attempted. In this sense, only a few studies have focused on the magnetoencephalographic (MEG) AD patterns. This work represents a new effort to explore the ability of three entropies from information theory to discriminate between spontaneous MEG rhythms from 20 AD patients and 21 controls. The Shannon (SSE), Tsallis (TSE), and Rényi (RSE) spectral entropies were calculated from the time-frequency distribution of the power spectral density (PSD). The entropies provided statistically significant lower values for AD patients than for controls in all brain regions (p < 0.0005). This fact suggests a significant loss of irregularity in AD patients' MEG activity. Maximal accuracy of 87.8% was achieved by both the TSE and RSE (90.0%, sensitivity; 85.7%, specificity). The statistically significant results obtained by both the extensive (SSE and RSE) and non-extensive (TSE) spectral entropies suggest that AD could disturb long and short-range interactions causing an abnormal brain function.

What are the benefits of cognitive enhancers for Alzheimer's Disease: use of Population Impact Measures

BackgroundThe study aims to quantify the population impact of prescribing cholinesterase inhibitors to slow the cognitive decline in Alzheimer's disease (AD), and to compare with the benefit of treating hypertension to prevent the onset of AD.MethodsLiterature review to ascertain the prevalence of AD, benefits of interventions, analysis of local and national surveys to measure the current use of interventions in the relevant population and application of the relevant findings to calculate Population Impact Measures. The Number of Events Prevented in a Population (NEPP) by the intervention over a defined time period is calculated for a UK urban population in one Local Authority (population size 217,000).ResultsTreatment of all eligible patients with mild to moderate AD with Cholinesterase Inhibitors would prevent cognitive deterioration (measured by ADAS – cog scale) in 123.6 (95% Confidence Intervals (CI) 82.3, 169.1), 16.4 (95% CI 2.1, 31.2) would show a mild improvement (4 points or more on the ADAS – cog scale) and 2.6 (95% CI 0.2, 5.8) would show an improvement of 7 points or more over a period of 6 months. This would require the treatment of 406 patients with Cholinesterase Inhibitors.Increasing from the current treatment rate of 46% of eligible patients to 'best practice' level would prevent cognitive deterioration in 66.8 (95% CI 44.0, 92.6), 8.99 (95% CI 1.2, 16.8) and 1.4 (95% CI 0.11, 3.2) would improve by 4 and 7 points respectively on the ADAS – cog scale over 6 months. This would require the treatment of an extra 187 patients with Cholinesterase Inhibitors beyond current practice, at an additional annual direct drug cost of £187,000.Improving the treatment of hypertension from current practice by 20% could prevent 8.2 (95% CI 2.3, 16.8) incident cases of AD in the next year. This would require the treatment of an extra 2711 patients with antihypertensive drugs.ConclusionPopulation Impact Measures are a new method to allow a demonstration of the magnitude of the benefit for the whole population following interventions. The use of drugs to slow cognitive decline, or to prevent AD by treating hypertension, can thus be assessed in a prioritisation exercise in competition with alternative use of resources.

Prevalence of Dementia in the United States: The Aging, Demographics, and Memory Study

Aim: To estimate the prevalence of Alzheimer’s disease (AD) and other dementias in the USA using a nationally representative sample. Methods: The Aging, Demographics, and Memory Study sample was composed of 856 individuals aged 71 years and older from the nationally representative Health and Retirement Study (HRS) who were evaluated for dementia using a comprehensive in-home assessment. An expert consensus panel used this information to assign a diagnosis of normal cognition, cognitive impairment but not demented, or dementia (and dementia subtype). Using sampling weights derived from the HRS, we estimated the national prevalence of dementia, AD and vascular dementia by age and gender. Results: The prevalence of dementia among individuals aged 71 and older was 13.9%, comprising about 3.4 million individuals in the USA in 2002. The corresponding values for AD were 9.7% and 2.4 million individuals. Dementia prevalence increased with age, from 5.0% of those aged 71–79 years to 37.4% of those aged 90 and older. Conclusions: Dementia prevalence estimates from this first nationally representative population-based study of dementia in the USA to include subjects from all regions of the country can provide essential information for effective planning for the impending healthcare needs of the large and increasing number of individuals at risk for dementia as our population ages.

The prevalence of dementia in the People's Republic of China: a systematic analysis of 1980–2004 studies

Dementia has been a major public health problem. However, there has not yet been a nationwide investigation or systematic analysis of the prevalence of dementia in China from 1980 to 2004. The aim of this study was to analyse the prevalence of dementia and its major subtypes [Alzheimer disease (AD), vascular dementia (VD)] among the population aged 60 years and older in China from 1980 to 2004. Epidemiological investigations on dementia in China published in journals and covering the period from 1980 to 2004 were identified manually and on-line by using CBMDISK, Chongqing VIP database and CNKI database. Those reported in English journals were identified using MEDLINE. Selected studies had to describe an original study defined by strict screening and diagnostic criteria. The fixed effects model or random effects model was employed according to statistical test for homogeneity. Twenty-five studies were selected, the statistical information of which was collected for systematic analysis. Our results showed that AD and VD were the two major subtypes of dementia in China, and the pooled prevalence of AD and VD for the population aged 60 years and older was 1.6 and 0.8%, respectively. There was a higher prevalence of AD in the illiterate elderly population (3.2%) than in those who received years of education. The chronological prevalence of AD increased significantly from 1980 to 2004. In southern and northern China, the prevalence of AD was 2.0 and 1.2%, respectively, while VD was 0.6 and 1.1%, respectively. In the last 24 years, AD and VD were the two major subtypes of dementia in China. The prevalence of AD may be affected by sex, education, occupation or age. The prevalence of VD, which was higher in northern than in southern China, seems not to be affected by age, sex or education.

Prevalence of Dementia Subtypes in El Prat de Llobregat, Catalonia, Spain: The PRATICON Study

Background: Studies on dementia subtypes show a wide variation in the prevalence of Alzheimer’s disease (AD) and vascular dementia (VD) worldwide. However, studies reporting on Lewy body dementia (LBD) and frontotemporal dementia (FTD) are sparse. Aims: To describe the prevalence ofdementia and subtypes. Method: A 34% sample of 5,150 subjects aged 70 years and over in El Prat de Llobregat (Barcelona) were screened by the Mini-Mental State Examination. When scoring <24, participants were assessed to establish a diagnosis. Results: There were 165 subjects diagnosed with dementia (prevalence of 9.4%). Subtypes of dementia were: AD 69.1%, VD 12.7%, LBD 9.1%, FTD 3% and secondary dementia 1.8%. Prevalences were: AD 6.5%, VD 1.2%, LBD 0.9% and FTD 0.3%. Conclusions: AD and VD were the most common type of dementia. Prevalence of dementia, AD and FTD were similar to those reported, while prevalence of VD and LBD were lower.

Now Is the Time to Prepare for the Onslaught of Alzheimer's Disease

Now Is the Time to Prepare for the Onslaught of Alzheimer's Disease

HOW COMMON ARE THE “COMMON” NEUROLOGIC DISORDERS?

To estimate the current incidence and prevalence in the United States of 12 neurologic disorders.We summarize the strongest evidence available, using data from the United States or from other developed countries when US data were insufficient.For some disorders, prevalence is a better descriptor of impact; for others, incidence is preferable. Per 1,000 children, estimated prevalence was 5.8 for autism spectrum disorder and 2.4 for cerebral palsy; for Tourette syndrome, the data were insufficient. In the general population, per 1,000, the 1-year prevalence for migraine was 121, 7.1 for epilepsy, and 0.9 for multiple sclerosis. Among the elderly, the prevalence of Alzheimer disease was 67 and that of Parkinson disease was 9.5. For diseases best described by annual incidence per 100,000, the rate for stroke was 183, 101 for major traumatic brain injury, 4.5 for spinal cord injury, and 1.6 for ALS.Using the best available data, our survey of a limited number of disorders shows that the burden of neurologic illness affects many millions of people in the United States.

Menopausal transition: A possible risk factor for brain pathologic events

Background and objective Incidence and prevalence of Alzheimer's disease (AD) are higher in postmenopausal women than in age-matched men. Since at menopause the endocrine system and other biological paradigms undergo substantial changes, we thought to be of interest studying whether (and how) the balance between some biological parameters allegedly neuroprotective (e.g. related to estrogen, dehydroepiandrosterone and CD36 functions) and others considered pro-neurotoxic (e.g. related to glucocorticoid and interleukin-6 activities) vary during lifespan in either sex in either normalcy or neurodegenerative disorders. Subjects and methods Along with this aim, we evaluated the gene expression levels of estrogen receptors (ERs), glucocorticoid receptors (HGRs), interleukin-6 (IL-6) and CD36, a scavenger receptor of class B allegedly playing a key role in the proinflammatory events associated with AD, in a population of 209 healthy subjects (73M, 106F, 20–91-year old) and 85 AD patients (36M, 49F, 65–89-year old). Results obtained were related to plasma titers of estrogens, cortisol and dehydroepiandrosterone sulfate (DHEAS). Studies were performed in peripheral leukocytes, since these cells (1) are easily obtainable by a simple blood sampling, (2) express many molecules and multiple receptors which are under the same regulatory mechanisms as those operative in the brain and (3) some of them, e.g. monocytes, share many functions with microglial cells. Results In healthy men all the study parameters were quite stable during lifespan. In women, instead, at menopausal transition, some changes that may predispose to neurodegeneration occurred. In particular, there was (1) an up-regulation of ERs, and a concomitant increase of IL-6 gene expression, events likely due to the loss of the inhibitory control exerted by estradiol (E 2); (2) an increase of HGRα:HGRβ ratio, indicative of an augmented cortisol activity on HGRα not sufficiently counteracted by the inhibitory HGRβ function; (3) a reduced CD36 expression, directly related to the increased cortisol activity; and (4) an augmented plasma cortisol:DHEAS ratio, widely recognized as an unfavorable prognostic index for the risk of neurodegeneration. In AD patients of both sexes, the expression of the study parameters was similar to that found in sex- and age-matched healthy subjects, thus indicating their unrelatedness to the disease, and rather a better correlation with biological events. Conclusions Menopausal transition is a critical phase of women's life where the occurrence of an unfavorable biological milieu would predispose to an increased risk of neurodegeneration. Collectively, the higher prevalence of AD in the female population would depend, at least in part, on the presence of favoring biological risk factors, whose contribution to the development of the disease occurs only in the presence of possible age-dependent triggers, such as beta-amyloid deposition.

Plasma 24S Hydroxycholesterol Response to Statins in Alzheimer’s Disease Patients: Effects of Gender, CYP46, and ApoE Polymorphisms

A number of epidemiologic studies suggest an association between plasma total cholesterol and risk for Alzheimer's disease (AD). Additionally, it has been suggested that treatment with statins, drugs that block cholesterol biosynthesis, lower the incidence and prevalence of AD and of vascular dementia. This review provides an overview of cholesterol transport within the central nervous system and the impact of statins on brain cholesterol metabolism in subjects with AD. Brain cholesterol is converted to 24-S-hydroxycholesterol, a reaction catalyzed by CYP46. The oxysterol traverses the blood-brain barrier and is transported to the liver by plasma lipoproteins. The levels of 24-S-hydroxy-cholesterol are a reflection of brain cholesterol turnover. Subjects with AD reportedly have high levels of the oxysterol possibly reflecting neuronal death with release of cell membrane cholesterol. We show gender dimorphism in plasma levels of 24-S-hydroxycholesterol in subjects with AD and significant reductions in plasma levels of the oxysterol during treatment with standard doses of statins (lovastatin, simvastatin, and pravastatin). Polymorphisms of apolipoprotein E and CYP46 do not influence the effect of statins on plasma levels of 24-S-hydroxycholesterol. There were no untoward effects of the standard doses of statin for the duration of treatment. Statins are currently in trial to determine their effect on the course of AD.

ALZHEIMER'S DISEASE MEDICATION: USE AND COST PROJECTIONS FOR MEDICARE PART D

ALZHEIMER'S DISEASE MEDICATION: USE AND COST PROJECTIONS FOR MEDICARE PART D