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All in the family: how the APPs regulate neurogenesis

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journal contribution
posted on 08.11.2013 by Orly Lazarov, Michael P. Demars
Recent intriguing evidence suggests that metabolites of amyloid precursor protein(APP), mutated in familial forms of Alzheimer’s disease(AD), play critical roles indevelopmental and post natal neurogenesis. Of note is soluble APPα (sAPPα) that regulates neural progenitor cell proliferation. The APP family encompasses a group of ubiquitously expressed and evolutionarily conserved, type I transmembrane glycoproteins, whose functions have yet to be fully elucidated. APP can undergo proteolytic cleavage by mutually exclusive pathways. The subtle structural differences between metabolites generated in the different pathways, as well as thei requilibrium, maybe crucial for neuronal function. The implications of this newbody of evidence are significant. Miscleavage of APP would readily impact developmental and postnatal neurogenesis, which might contribute to cognitive deficits characterizing Alzheimer’s disease. This review will discuss the implications of the role of the APP family in neurogenes is for neuronal development, cognitive function, and brain disorders that compromise learning and memory, such as AD.

Funding

The work was supported by the NIA AG033570 (Orly Lazarov), Alzheimer’s Association Young Investigator Award (Orly Lazarov), the Illinois Department of Public Health ADRF award (Orly Lazarov),and the Brain Research Foundation (Orly Lazarov).

History

Publisher Statement

This Document is Protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.

Publisher

Frontiers

Language

en_US

issn

1662-453X

Issue date

01/06/2012

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