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

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

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J-P. Michel et al. 1% TABLE IV: Relation of cognitive status at admission and neuropathological diagnosis in 52 autopsied diabetic patients. It appears, therefore, that diabetics presenting with lesions of Alzheimer type display clinically cognitive dysfunction in the form of poor intellectual performance (MMSE<21) in only 43% of cases. DISCUSSION This study is unique insofar as, to our knowledge, it is the first to attempt to establish a correlation between diabetes and dementia based upon neuropathology.

1964). It was suggested that the microglia might be changing amyloid from non fibrillar substrates to the extracellular filamentous form, as subsequently R. D. Terry 22 elaborated by Wisniewski and Wegiel (1994). A major normal function of microglia is to remodel synapses. Degenerative synapses might well activate the microglia and begin the cascade of events involving the cytokines and complement. Of course, many other hypotheses have been suggested for etiology, primacy, and pathogenesis of AD in addition to amyloid, tau, axoplasmic flow and inflammation.

J Bioi Chern 266:22019-22027. Scheibel ME, Lindsay RD, Tomiyasu U and Scheibel AB (1976): Progressive dendritic changes in the aging human limbic system. Exp NeuroI53:420-430. Singh TJ, Grundke-Iqbal I and Iqbal K (1996): Differential phosphorylation of human tau isoforms containing three repeats by several protein kinases. Arch Biochern Biophys. In Press. Wang J-Z, Gong CoX, Zaidi T, Grundke-Iqbal I and Iqbal K (1995): Dephosphorylation of Alzheimer paired helical filaments by protein phosphatase2A and -2B.

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