Alzheimer’s Disease. Epidemiology, Neuropathology, by Dr. R. J. Wurtman (auth.), Prof. Dr. Konrad Maurer, Prof.

By Dr. R. J. Wurtman (auth.), Prof. Dr. Konrad Maurer, Prof. Dr. Peter Riederer, Prof. Dr. Helmut Beckmann (eds.)

The ebook Alzheimer's disorder - Epidemiology, Neuropathology,Neurochemistry, and Clinics is derived from a world Symposium at the party of the a hundred and twenty fifth Anniversary of the delivery of Alois Alzheimer (14.6.1864-19.12.1915). during the last decade, because the aged became the fastest-growing phase of the inhabitants in industrialized nations, Alzheimer's sickness has emerged as one of many significant psychological illnesses. The individuals to this booklet symbolize the world over well-known professionals within the box of dementia and current new information regarding epidemiology, neuropathology, neurochemistry, and clinics in Alzheimer's sickness. This ebook is a wealthy and priceless up to date source for psychiatrists, neurologists, scientists operating within the fields of neuropathology, neurochemistry and molecular genetics, behavioral scientists, relatives physicians and all who proportion an curiosity in knowing and treating the older person with Alzheimer's disease/dementia.

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Additional info for Alzheimer’s Disease. Epidemiology, Neuropathology, Neurochemistry, and Clinics

Sample text

Neither was there conclusive evidence for an association with prior viral diseases Qr possible sources of viral infections, as Amaducci et al. (1986) stated in their analysis of possible risk factors for Alzheimer's disease. 8 years, Bickel and Cooper (1989) applied the "proportional hazard Epidemiology of Alzheimer's disease 35 regression model" of Cox and found that neither severe physical impairment nor low social status and living alone had a significant influence on the risk of developing dementia.

G. Amaducci before the age of70). In late-onset cases Chandra et al. (1987) found no increase in SDAT among family members. However, with respect to the sources of error mentioned, the findings are not yet sufficient to give a clear picture of the strength of genetic determination in relation to age of onset, although very young age of onset is likely to be associated with a stronger genetic load. In view of the unimodal, exponential distribution across age of the risk of first onset, the early Kraepelinian assumption of two diseases, the Mendelian inherited presenile dementia and a non-inherited senile dementia, must be considered unlikely.

There is, however, a marked variation of the sex ratios for both types of dementia, as shown in Table 3, which, up to now, does not allow to draw firm conclusions. J orm et al. (1988) developed a quantitative model providing detailed estimates of the prevalence rates for dementia on the basis of population projections up to the year 2025. 73% by 2025 (see Table 4). If this estimate were to come true, we would have to reckon with a number of 850000 dementia sufferers in 2025. About 590 000 of these would suffer from Alzheimer's disease partly combined with vascular dementia (Table 5).

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