NDLI: Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models.

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Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tatsuno, G. Nicoll, R. A. Mcconlogue, L. Hu, K. Yu, G. Q. Mucke, L. Hsia, A. Y. Masliah, E. Malenka, R. C. Kholodenko, D.
Description	Author Affiliation: Hsia AY ( Department of Cellular and Molecular Pharmacology, University of California at San Francisco, San Francisco, CA 94143-0450, USA.);
Abstract	Autosomal dominant forms of familial Alzheimer's disease (FAD) are associated with increased production of the amyloid beta peptide, Abeta42, which is derived from the amyloid protein precursor (APP). In FAD, as well as in sporadic forms of the illness, Abeta peptides accumulate abnormally in the brain in the form of amyloid plaques. Here, we show that overexpression of FAD(717V-->F)-mutant human APP in neurons of transgenic mice decreases the density of presynaptic terminals and neurons well before these mice develop amyloid plaques. Electrophysiological recordings from the hippocampus revealed prominent deficits in synaptic transmission, which also preceded amyloid deposition by several months. Although in young mice, functional and structural neuronal deficits were of similar magnitude, functional deficits became predominant with advancing age. Increased Abeta production in the context of decreased overall APP expression, achieved by addition of the Swedish FAD mutation to the APP transgene in a second line of mice, further increased synaptic transmission deficits in young APP mice without plaques. These results suggest a neurotoxic effect of Abeta that is independent of plaque formation.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	6
Volume Number	96
Language	English
Publisher	National Academy of Sciences
Publisher Date	1999-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Alzheimer Disease Pathology Amyloid Beta-Peptides Metabolism Brain Nerve Net Genetics Physiopathology Amyloid Beta-Protein Precursor Biosynthesis Animals Disease Models, Animal Electrophysiology Mice Mice, Transgenic Mutation 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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