Prevalence of AD among whites

Hy, Lê Xuân; Keller, Donald M.

doi:10.1212/wnl.55.2.198

Cited by 137 publications

(77 citation statements)

References 34 publications

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“…Nevertheless, we believe the two stage model of disease progression used here, produces useful estimates of the numbers of patients requiring a high level of care roughly equivalent to that provided by a health care facility such as a nursing home. Epidemiological surveys of the percentage of cases with severe disease have ranged between 2% to over 50% (14)(15)(16). Such wide variation could result either from differences in survey methodology and diagnostic criteria, or sampling enrollment biases.…”

Section: Discussionmentioning

confidence: 99%

Forecasting the global burden of Alzheimer's disease

Brookmeyer

Johnson

Ziegler-Graham

et al. 2007

Alzheimer's & Dementia

2,892

1,908

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Section: Discussionmentioning

confidence: 99%

Forecasting the global burden of Alzheimer's disease

Brookmeyer

Johnson

Ziegler-Graham

et al. 2007

Alzheimer's & Dementia

2,892

1,908

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show abstract

“…For example, some studies include persons with incipient dementia, others include mild dementia, and still others only included individuals with moderate to severe dementia. 5,6 As an example of the effect of such difference, two studies of largely white cohorts in the northeastern United States generated widely disparate incidence rates. The age-specific annual incidence rates for AD in the group aged 60 to 65 was 0.6% per year in the East Boston study.…”

Section: Analysis Of Evidence Does the Presence Of Mild Cognitive Immentioning

confidence: 99%

Practice parameter: Early detection of dementia: Mild cognitive impairment (an evidence-based review) [RETIRED]

et al. 2001

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Article abstract-Objective: The goal of this project was to determine whether screening different groups of elderly individuals in a general or specialty practice would be beneficial in detecting dementia. Background: Epidemiologic studies of aging and dementia have demonstrated that the use of research criteria for the classification of dementia has yielded three groups of subjects: those who are demented, those who are not demented, and a third group of individuals who cannot be classified as normal or demented but who are cognitively (usually memory) impaired. Methods: The authors conducted computerized literature searches and generated a set of abstracts based on text and index words selected to reflect the key issues to be addressed. Articles were abstracted to determine whether there were sufficient data to recommend the screening of asymptomatic individuals. Other research studies were evaluated to determine whether there was value in identifying individuals who were memory-impaired beyond what one would expect for age but who were not demented. Finally, screening instruments and evaluation techniques for the identification of cognitive impairment were reviewed. Results: There were insufficient data to make any recommendations regarding cognitive screening of asymptomatic individuals. Persons with memory impairment who were not demented were characterized in the literature as having mild cognitive impairment. These subjects were at increased risk for developing dementia or AD when compared with similarly aged individuals in the general population. Recommendations: There were sufficient data to recommend the evaluation and clinical monitoring of persons with mild cognitive impairment due to their increased risk for developing dementia (Guideline). Screening instruments, e.g., Mini-Mental State Examination, were found to be useful to the clinician for assessing the degree of cognitive impairment (Guideline), as were neuropsychologic batteries (Guideline), brief focused cognitive instruments (Option), and certain structured informant interviews (Option). Increasing attention is being paid to persons with mild cognitive impairment for whom treatment options are being evaluated that may alter the rate of progression to dementia.

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“…In addition, lack of education is found to be negatively associated with AD risk. However, the female prevalence in AD remains after adjusting for age and education (24)(25)(26) and female hormone may, in part, also contribute to gender-related differences in AD. After menopause, the decline of estrogen levels in the brain may make neurons more susceptible to age-related neurodegenerative processes (27).…”

mentioning

confidence: 99%

Brain estrogen deficiency accelerates Aβ plaque formation in an Alzheimer's disease animal model

Yue

Lu²,

Lancaster³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

334

306

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Much evidence indicates that women have a higher risk of developing Alzheimer's disease (AD) than do men. The reason for this gender difference is unclear. We hypothesize that estrogen deficiency in the brains of women with AD may be a key risk factor. In rapidly acquired postmortem brains from women with AD, we found greatly reduced estrogen levels compared with those from age-and gender-matched normal control subjects; AD and control subjects had comparably low levels of serum estrogen. We examined the onset and severity of AD pathology associated with estrogen depletion by using a gene-based approach, by crossing the estrogen-synthesizing enzyme aromatase gene knockout mice with APP23 transgenic mice, a mouse model of AD, to produce estrogen-deficient APP23 mice. Compared with APP23 transgenic control mice, estrogen-deficient APP23 mice exhibited greatly reduced brain estrogen and early-onset and increased ␤ amyloid peptide (A␤) deposition. These mice also exhibited increased A␤ production, and microglia cultures prepared from the brains of these mice were impaired in A␤ clearance͞degradation. In contrast, ovariectomized APP23 mice exhibited plaque pathology similar to that observed in the APP23 transgenic control mice. Our results indicate that estrogen depletion in the brain may be a significant risk factor for developing AD neuropathology.amyloid deposition ͉ aromatase ͉ transgenic animal N europathological hallmarks of Alzheimer's disease (AD) include significant deposition of extracellular ␤ amyloid peptide (A␤) and presence of neurofibrillary tangles in the brain (1). A␤ is derived from the two-step enzymatic processing of amyloid precursor protein (APP) in which ␤-secretase (BACE) cleaves the ␤-site of APP to release the N terminus of A␤, and the ␥-secretase protein complex cleaves the ␥-site of APP to release the C terminus of A␤ (2, 3). Overproduction and progressive deposition of A␤ are known to underlie, in part, A␤ plaque formation, a key pathologic feature of AD. The initial cleavage of APP by BACE is critical for A␤ associated with AD neuropathology (4). Recent studies have shown that BACE activity increases with age and is elevated in AD brains (5, 6).Impaired A␤ clearance and͞or degradation may also contribute to A␤ plaque formation. Our previous findings support this hypothesis: Microglia isolated from AD brains have impaired phagocytic activity, leading to reduced A␤ clearance (7). Other groups have found that cytoplasmic A␤ granules in the plaque-associated glia and microglia participate in the clearance of A␤ in A␤-immunized AD patients and APP transgenic mice (8, 9).Two enzymes are involved in A␤ degradation and clearance: insulin-degrading enzyme (IDE) and neprilysin (NEP). IDE is expressed in high concentrations in the brain. Besides degrading insulin and several regulatory peptides, IDE also degrades the intracellular domain of APP and is responsible for degrading and clearing A␤ from the brain (10, 11). Indeed, genetic linkage studies have shown that late-onset AD loci on chromosome 1...

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Prevalence of AD among whites

Cited by 137 publications

References 34 publications

Forecasting the global burden of Alzheimer's disease

Forecasting the global burden of Alzheimer's disease

Practice parameter: Early detection of dementia: Mild cognitive impairment (an evidence-based review) [RETIRED]

Brain estrogen deficiency accelerates Aβ plaque formation in an Alzheimer's disease animal model

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