Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model.

Abstract	Many potential treatments for Alzheimer's disease target amyloid-beta peptides (Abeta), which are widely presumed to cause the disease. The microtubule-associated protein tau is also involved in the disease, but it is unclear whether treatments aimed at tau could block Abeta-induced cognitive impairments. Here, we found that reducing endogenous tau levels prevented behavioral deficits in transgenic mice expressing human amyloid precursor protein, without altering their high Abeta levels. Tau reduction also protected both transgenic and nontransgenic mice against excitotoxicity. Thus, tau reduction can block Abeta- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer's disease and related conditions.
Authors	Erik D Roberson, Kimberly Scearce-Levie, Jorge J Palop, Fengrong Yan, Irene H Cheng, Tiffany Wu, Hilary Gerstein, Gui-Qiu Yu, Lennart Mucke
Journal	Science (New York, N.Y.) (Science) Vol. 316 Issue 5825 Pg. 750-4 (May 04 2007) ISSN: 1095-9203 [Electronic] United States
PMID	17478722 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References	Amyloid beta-Peptides Amyloid beta-Protein Precursor Convulsants Excitatory Amino Acid Agonists tau Proteins Kainic Acid Pentylenetetrazole
Topics	Alzheimer Disease (metabolism, pathology, physiopathology, therapy) Amyloid beta-Peptides (metabolism) Amyloid beta-Protein Precursor (genetics, metabolism) Animals Axons (ultrastructure) Convulsants (pharmacology) Disease Models, Animal Excitatory Amino Acid Agonists (pharmacology) Exploratory Behavior Hippocampus (pathology) Humans Kainic Acid (pharmacology) Maze Learning Memory Mice Mice, Inbred C57BL Mice, Transgenic Motor Activity Pentylenetetrazole (pharmacology) Phosphorylation Seizures (prevention & control) tau Proteins (genetics, metabolism)

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