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P3‐414: Peripheral expression of neprilysin leads to clearance of brain Abeta
Author(s) -
Hersh Louis B.,
Studzinski Christa,
Beckett Tina,
Murphy M. Paul,
Klein Ronald L.,
Liu Yinxing
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.1957
Subject(s) - neprilysin , peptide , amyloid (mycology) , amyloid beta , chemistry , medicine , endocrinology , biochemistry , enzyme , inorganic chemistry
impairment of cognitive function. Conclusions: Our studies provide strong evidence that the N-termini of amyloid peptides influence their characteristics. This is primarily caused by a loss of N-terminal charge and solubility which increases aggregation propensity and, interestingly, influence on LTP. Likewise, novel transgenic animal models overproducing N-truncated Abeta develop an early phenotype. Thus, an accumulation of N-truncated amyloid as described for human AD might contribute to the pathogenesis due to the changes in the molecular properties. The data suggest that suppression of QC-catalyzed pGlu-formation provides potential for development of a treatment paradigm to prevent Aband inflammation-driven pathophysiology in AD, FDD and FBD.