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By Howard Feldman

Authored by way of one of many world's major gurus at the administration of Alzheimer's illness and similar dementias, this hugely illustrated atlas describes the colourful background of Alzheimer's illness; its neuropathological foundation from structural mind imaging and autopsy reviews; and its devastating results on belief, cognition, conversation, and social habit. The booklet also will position nice emphasis at the more and more identifiable probability elements for improvement of the affliction, with a view in the direction of prevention.

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Extra resources for Atlas of Alzheimer's Disease

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By contrast, the observed decrease in prevalence of vascular dementia is hypothesized to be due to a lower incidence with improved preventive measures as health awareness in the society progressed. Incidence of dementia and Alzheimer’s disease While a large number of prevalence studies on dementia have been done, especially in the developed world, incidence studies are less frequent, probably because they are much more costly to conduct. 6,33–40 The variation in the findings among different parts of the world, and sometimes even within a country, may be due to a number of reasons.

Qxp 5/12/2007 11:26 AM Page 34 AT L A S O F A L Z H E I M E R ’ S D I S E A S E 100 90 80 Surviving, % 80 Incidence rate per 1000 person-years Age <75 years Age <75–84 years Age <85 years 70 60 50 60 40 20 40 0 2 4 6 8 10 No. 11 Survival after diagnosis of AD by age of onset. (Reprinted from Brookmeyer et al. Survival following a diagnosis of Alzheimer disease. 49 Copyright  2002, American Medical Association. All rights reserved). 12 Cumulative hazard of death as a function of time, stratified by quartiles according to rate of cognitive decline.

17e). 22 During this period of molecular discovery, genetic risk factors for both familial and sporadic forms of AD were identified. Apolipoprotein E (ApoE) gene polymorphisms were shown to be involved in late-onset familial cases of AD. 17f). To date, no mutations in the tau gene have been associated with familial AD. However, neurofibrillary tangle pathology appears to play an important role in AD progression. Mutations in the tau gene on chromosome 17 have been associated with the class of frontotemporal dementias with parkinsonism (FTDP-17).

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