Download Alzheimer Disease: From Molecular Biology to Theraphy by Luigi Amaducci, Marzia Baldereschi (auth.), Robert E. PDF

By Luigi Amaducci, Marzia Baldereschi (auth.), Robert E. Becker, Ezio Giacobini, Joyce M. Barton, Mona Brown (eds.)

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Extra info for Alzheimer Disease: From Molecular Biology to Theraphy

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It is, however, increasingly clear that there are logical problems in both positions. Table II cites several circumstances in which ~-amyloid is present without tangles and therefore, this amyloid does not necessarily induce tangles. There are other instances where tangles are present without amyloid; and so tangles do not necessarily lead to the formation of amyloid. There must be other factors involved in Alzheimer disease (AD). Some of the argument on pathogenesis has been based on which lesion came first.

0% of brains devoid of macroscopic and microscopic lesions. 1%, respectively. 0% of brains devoid of macroscopic and microscopic lesions. Matching of the above neuropathologic results against the cognitive status of patients from the 3 groups considered (NIDDM, IGT and normoglycemics) produces highly interesting results. 2% had MD lesions (Table IV). 4% had MD lesions (Table IV). J-P. Michel et al. 1% TABLE IV: Relation of cognitive status at admission and neuropathological diagnosis in 52 autopsied diabetic patients.

Wilson PW, Keaven M, Anderson PD (1986): Epidemiology of diabetes mellitus in the elderly. The Framingham study.

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