Prolonged Abeta treatment leads to impairment in the ability of primary cortical neurons to maintain K+ and Ca2+ homeostasis.

ABSTRACT:

Background

Alzheimer's disease (AD) is a progressive neurodegenerative disease, characterised by the formation of insoluble amyloidogenic plaques and neurofibrillary tangles. Beta amyloid (Abeta) peptide is one of the main constituents in Abeta plaques, and is thought to be a primary causative agent in AD. Neurons are likely to be exposed to chronic, sublethal doses of Abeta over an extended time during the pathogenesis of AD, however most studies published to date using in vitro models have focussed on acute studies. To experimentally model the progressive pathogenesis of AD, we exposed primary cortical neurons daily to 1 muM of Abeta1-40 over 7 days and compared their survival with age-similar untreated cells. We also investigated whether chronic Abeta exposure affects neuronal s

SUBMITTER: Shabala L 

PROVIDER: S-EPMC2927593 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature