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Ovsepian, S.V.* ; O'Leary, V.B.

Neuronal activity and amyloid plaque pathology: An update.

J. Alzheimers Dis. 49, 13-19 (2015)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
A breakthrough in Alzheimer's disease (AD) research came with the discovery of the link between activity-dependent release of amyloid-β (Aβ) from neurons and formation of amyloid plaques. Along with elucidating the cellular basis of behavioral-dependent fluctuations in Aβ levels in the brain, insights have been gained toward understanding the mechanisms that warrant selective vulnerability of various forebrain circuits to amyloid pathology. The notion of elevated activity as a source of excessive Aβ production and plaque formation is, however, in conflict with ample electrophysiological data, which demonstrate exceedingly intense activity (both intrinsic and synaptic) of neurons in several brain regions that are spared or marginally affected by amyloid plaques of AD. Thus, the link between the functional load of brain circuits and their vulnerability to amyloidosis, while evident, is also complex and remains poorly understood. Here, we discuss emerging data suggestive of a major role for super-intense synchronous activity of cortical and limbic networks in excessive Aβ production and plaque formation. It is proposed that dense recurrent wiring of associative areas prone to epileptic seizures might be of critical relevance to their higher susceptibility to plaque pathology and related functional impairments.
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Publication type Article: Journal article
Document type Review
Corresponding Author
Keywords Alzheimer’s Disease ; Amyloid-β Peptide ; Hetero-modal Associative Cortex ; Neuronal Synchrony ; Non-convulsive Seizure
ISSN (print) / ISBN 1387-2877
e-ISSN 1875-8908
Journal Journal of Alzheimer's Disease
Quellenangaben Volume: 49, Issue: 1, Pages: 13-19 Article Number: , Supplement: ,
Publisher IOS Press
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Radiation Biology (ISB)