The most common causes of neurodegenerative dementia include Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). We believe that, in all 3, aggregates of pathogenic proteins are pathological substrates which are associated with a loss of synaptic function/plasticity. The synaptic plasticity relies on the normal integration of glutamate receptors at the postsynaptic density (PSD). The PSD organizes synaptic proteins to mediate the functional and structural plasticity of the excitatory synapse and to maintain synaptic homeostasis. Here, we will discuss the relevant disruption of the protein network at the PSD in these dementias and the accumulation of the pathological changes at the PSD years before clinical symptoms. We suggest that the functional and structural plasticity changes of the PSD may contribute to the loss of molecular homeostasis within the synapse (and contribute to early symptoms) in these dementias.
Disruption of the Postsynaptic Density in Alzheimer's Disease and Other Neurodegenerative Dementias
Creators
Yuesong Gong - Drexel University
Carol F. Lippa - Drexel University
Publication Details
American journal of Alzheimer's disease and other dementias, v 25(7), pp 547-555
Publisher
Sage
Number of pages
9
Grant note
R21AG031388 / NATIONAL INSTITUTE ON AGING; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute on Aging (NIA)
Potamkin Foundation
Resource Type
Journal article
Language
English
Web of Science ID
WOS:000282645000002
Scopus ID
2-s2.0-77957954675
Other Identifier
991019312378604721
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Web of Science research areas
Clinical Neurology
Geriatrics & Gerontology
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