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P2‐181: Oxidative lipid modification of nicastrin enhances Aβ production in Alzheimer's disease
Author(s) -
Jo DongGyu,
Choi YunHyung,
Gwon ARyeong,
Mattson Mark P.
Publication year - 2009
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.2009.04.493
Subject(s) - nicastrin , lipid peroxidation , oxidative stress , 4 hydroxynonenal , chemistry , lipid raft , biochemistry , genetically modified mouse , amyloid precursor protein , presenilin , microbiology and biotechnology , alzheimer's disease , transgene , biology , cell , medicine , disease , gene
key role which might be considered as an adjunct therapeutic strategy to combat neural demise in AD and other oxidative stress-related disease. The viability and cell cytotoxicity assays demonstrated that in presence of alginate the amount of cell death and caspase-3 activation diminished significantly in NT2 neurons. Besides, in contrast to most other Nrf2-activators like flavonoids, sulforaphane or curcumin which are already toxic at low concentration, alginate however showed no toxicity in our assays in vitro and thereby shows chaperone-like activity at low concentrations. Conclusions: This study provides the first documentation of the neuroprotective and chaperone-like activity of alginate through suppression of Ab formation. Therefore use of alginate might be considered as an adjunct therapeutic strategy to combat neural demise in AD.