Read e-book online Alzheimer Disease: From Molecular Biology to Theraphy PDF

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

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1994) areas and is significant in the neuropil between as well as within plaques. The loss of synapses is greater than that of neurons. Given the prominence of the two major (and oldest) findings -plaques and tangles- it is not surprising that there are two major opposing concepts 20 R. D. Terry POSITIVE • Plaques & Amyloid • Tangles & PHF • Neuropil Threads • Activated Microglia TABLE I: Structural changes in AD NEGATIVE • Neuron Loss • Synapse Loss concerning the primary element of the pathogenesis.

1995) .. Ten of the twenty-one sites are canonical sites for the proline-directed protein kinases (PDPKs) and the remaining eleven are the non-PDPK sites. , 1996). Thus, probably several protein kinases are involved in the phosphorylation of tau. However, to date, neither the exact identification of the protein kinases nor the sequence in which they phosphorylate tau to an Alzheimer-like state is fully understood. Furthermore, currently there is no clear evidence for the upregulation of the activity of any tau kinase(s) in AD brain.

1990): The mental efficiency of the elderly person with type II diabetes mellitus. JAm Geriatr Soc 38:505-10. Wade JPH, Hachinski VC (1987): Multi-infarct dementia In: Dementia. Churchill, Livingstone, Edinburgh, eds. PITT B 209-28. WHO (1985): Diabetes mellitus. Technical report 727, WHO Geneva. Wilson PW, Keaven M, Anderson PD (1986): Epidemiology of diabetes mellitus in the elderly. The Framingham study.

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