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Alzheimer z disease advances in etiology, pathogenesis a - download pdf or read online

By Khalid Iqbal, Sangram S. Sisodia, Bengt Winblad

ISBN-10: 0470846453

ISBN-13: 9780470846452

ISBN-10: 0471521760

ISBN-13: 9780471521761

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This conformational/aggregational transformation could also result from changes in pH, local concentration, lack of clearance and interaction with other molecules, which he terms ‘pathological chaperones’, and he identified apolipoprotein E (apoE) as one of these long before linkage analysis demonstrated an association between apoE and late onset FAD and sporadic AD. Dr Frangione began his research career as a physician in Buenos Aires. He worked at New York University Medical Center before going to Cambridge, UK, where he received his PhD.

Subsequent studies by Dr Grundke-Iqbal and her colleagues demonstrated that the levels of tau in abnormally hyperphosphorylated form are increased several-fold in Alzheimer’s disease, and that the mechanism of the neurofibrillary degeneration, a key lesion in Alzheimer’s disease, involves the sequestration of normal microtubule-associated proteins and disassembly of microtubules by the abnormally hyperphosphorylated tau. She and her colleagues also discovered: (1) that the abnormal phosphorylation of tau precedes its polymerization into paired helical filaments and incorporation of ubiquitin; (2) that the levels of conjugated ubiquitin are elevated in both the brains and cerebrospinal fluids of patients with Alzheimer’s disease; (3) that there is a significant pool of soluble abnormally phosphorylated tau in Alzheimer’s disease brain; (4) that the abnormally phosphorylated tau is three- to four-fold more phosphorylated than the normal brain tau; and (5) that by dephosphorylation in vitro, paired helical filaments dissociate, the tau released has normal microtubule assemblypromoting activity, and protein phosphatase-2A is a major regulator of the phosphorylation of tau.

1987). 1. In this figure, the log of age-specific dementia prevalence is plotted against age. 1. 7 million in 2050. Most of the increase is attributable to the aging of the population that will occur in the next 50 years. This extraordinary increase would be mitigated if we learned how to delay the onset of AD. Khatchaturian Alzheimer’s Disease: Advances in Etiology, Pathogenesis and Therapeutics. Edited by K. Iqbal, S. S. Sisodia & B. Winblad. & 2001 John Wiley & Sons, Ltd. 1. Prevalence of age-specific dementia (as log prevalence of age-defined population) plotted against age.

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Alzheimer z disease advances in etiology, pathogenesis a therapeutics by Khalid Iqbal, Sangram S. Sisodia, Bengt Winblad

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