By Khalid Iqbal (Editor), Sangram S. Sisodia (Editor), Bengt Winblad (Editor)
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Extra resources for Alzheimer's Disease: Advances in Etiology, Pathogenesis and Therapeutics
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.
Psychiatry Clin Neurosci 52(suppl), S291–4. edu Alzheimer’s Disease: Advances in Etiology, Pathogenesis and Therapeutics Edited by Khalid Iqbal, Sangram S. , 1994).
1990). Similar results were obtained in the large study carried out in Bordeaux. Incidence data are now available. , 2000). An evident explanation of the protective effect of education is that education increases cognitive reserve, thus delaying the onset of the clinical symptoms of dementia (Katzman and Kawas, 1999). , 1999). However, in Indianapolis, Hall et al. (2000) found that lack of education is of greater importance in reducing dementia in African Americans who grew up in rural areas, not in those who grew up in cities.
Alzheimer's Disease: Advances in Etiology, Pathogenesis and Therapeutics by Khalid Iqbal (Editor), Sangram S. Sisodia (Editor), Bengt Winblad (Editor)