NDLI: Tau is essential to beta -amyloid-induced neurotoxicity.

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Tau is essential to beta -amyloid-induced neurotoxicity.

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Tau is essential to beta -amyloid-induced neurotoxicity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ferreira, Adriana Dawson, Hana N. Rapoport, Mark Binder, Lester I. Vitek, Michael P.
Description	Author Affiliation: Rapoport M ( Institute for Neuroscience, Northwestern University, Chicago, IL 60611, USA.);
Abstract	Senile plaques and neurofibrillary tangles, the two hallmark lesions of Alzheimer's disease, are the results of the pathological deposition of proteins normally present throughout the brain. Senile plaques are extracellular deposits of fibrillar beta-amyloid peptide (Abeta); neurofibrillary tangles represent intracellular bundles of self-assembled hyperphosphorylated tau proteins. Although these two lesions are often present in the same brain areas, a mechanistic link between them has yet to be established. In the present study, we analyzed whether tau plays a key role in fibrillar Abeta-induced neurite degeneration in central neurons. Cultured hippocampal neurons obtained from wild-type, tau knockout, and human tau transgenic mice were treated with fibrillar Abeta. Morphological analysis indicated that neurons expressing either mouse or human tau proteins degenerated in the presence of Abeta. On the other hand, tau-depleted neurons showed no signs of degeneration in the presence of Abeta. These results provide direct evidence supporting a key role for tau in the mechanisms leading to Abeta-induced neurodegeneration in the central nervous system. In addition, the analysis of the composition of the cytoskeleton of tau-depleted neurons suggested that the formation of more dynamic microtubules might confer resistance to Abeta-mediated neurodegeneration.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	9
Volume Number	99
Language	English
Publisher	National Academy of Sciences
Publisher Date	2002-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Amyloid Beta-Peptides Metabolism Brain Central Nervous System Tau Proteins Physiology Animals Blotting, Western Cytoskeleton Hippocampus Immunoblotting Immunohistochemistry Mice Mice, Knockout Mice, Transgenic Microtubules Phenotype Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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