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ABSTRACT: Background
The serine/threonine protein phosphatase, PP2A, is thought to play a central role in the molecular pathogenesis of Alzheimer's disease (AD), and the activity and substrate specificity of PP2A is regulated, in part, through methylation and demethylation of its catalytic subunit. Previously, we found that transgenic overexpression of the PP2A methyltransferase, LCMT-1, or the PP2A methylesterase, PME-1, altered the sensitivity of mice to impairments caused by acute exposure to synthetic oligomeric amyloid-β (Aβ).Objective
Here we sought to test the possibility that these molecules also controlled sensitivity to impairments caused by chronically elevated levels of Aβ produced in vivo.Methods
To do this, we examined the effects of transgenic LCMT-1, or PME-1
SUBMITTER: Gnanaprakash M
PROVIDER: S-EPMC8203222 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature