Document Detail


Neprilysin-sensitive synapse-associated amyloid-beta peptide oligomers impair neuronal plasticity and cognitive function.
MedLine Citation:
PMID:  16636059     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A subtle but chronic alteration in metabolic balance between amyloid-beta peptide (Abeta) anabolic and catabolic activities is thought to cause Abeta accumulation, leading to a decade-long pathological cascade of Alzheimer disease. However, it is still unclear whether a reduction of the catabolic activity of Abeta in the brain causes neuronal dysfunction in vivo. In the present study, to clarify a possible connection between a reduction in neprilysin activity and impairment of synaptic and cognitive functions, we cross-bred amyloid precursor protein (APP) transgenic mice (APP23) with neprilysin-deficient mice and biochemically and immunoelectron-microscopically analyzed Abeta accumulation in the brain. We also examined hippocampal synaptic plasticity using an in vivo recording technique and cognitive function using a battery of learning and memory behavior tests, including Y-maze, novel-object recognition, Morris water maze, and contextual fear conditioning tests at the age of 13-16 weeks. We present direct experimental evidence that reduced activity of neprilysin, the major Abeta-degrading enzyme, in the brain elevates oligomeric forms of Abeta at the synapses and leads to impaired hippocampal synaptic plasticity and cognitive function before the appearance of amyloid plaque load. Thus, reduced neprilysin activity appears to be a causative event that is at least partly responsible for the memory-associated symptoms of Alzheimer disease. This supports the idea that a strategy to reduce Abeta oligomers in the brain by up-regulating neprilysin activity would contribute to alleviation of these symptoms.
Authors:
Shu-Ming Huang; Akihiro Mouri; Hideko Kokubo; Ryuichi Nakajima; Takahiro Suemoto; Makoto Higuchi; Matthias Staufenbiel; Yukihiro Noda; Haruyasu Yamaguchi; Toshitaka Nabeshima; Takaomi C Saido; Nobuhisa Iwata
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-04-24
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  281     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-26     Completed Date:  2006-08-18     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  17941-51     Citation Subset:  IM    
Affiliation:
Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.
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MeSH Terms
Descriptor/Qualifier:
Alzheimer Disease / metabolism,  pathology,  physiopathology*
Amyloid beta-Protein / genetics,  metabolism*
Animals
Cognition / physiology*
Female
Hippocampus / metabolism,  pathology,  physiopathology
Male
Maze Learning / physiology
Memory / physiology
Mice
Mice, Transgenic
Microscopy, Electron
Neprilysin / genetics,  metabolism*
Neuronal Plasticity / physiology*
Peptide Fragments / metabolism
Synapses / pathology,  physiology,  ultrastructure
Chemical
Reg. No./Substance:
0/Amyloid beta-Protein; 0/Peptide Fragments; EC 3.4.24.11/Neprilysin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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