Amyloid Precursor Protein Translation Is Regulated by a 3'UTR Guanine Quadruplex.

ABSTRACT: A central event in Alzheimer's disease is the accumulation of amyloid β (Aβ) peptides generated by the proteolytic cleavage of the amyloid precursor protein (APP). APP overexpression leads to increased Aβ generation and Alzheimer's disease in humans and altered neuronal migration and increased long term depression in mice. Conversely, reduction of APP expression results in decreased Aβ levels in mice as well as impaired learning and memory and decreased numbers of dendritic spines. Together these findings indicate that therapeutic interventions that aim to restore APP and Aβ levels must do so within an ideal range. To better understand the effects of modulating APP levels, we explored the mechanisms regulating APP expression focusing on post-transcriptional regulation. Such regulation can

SUBMITTER: Crenshaw E 

PROVIDER: S-EPMC4664259 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature