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Disruption of the Postsynaptic Density in Alzheimer's Disease and Other Neurodegenerative Dementias
Journal article   Open access   Peer reviewed

Disruption of the Postsynaptic Density in Alzheimer's Disease and Other Neurodegenerative Dementias

Yuesong Gong and Carol F. Lippa
American journal of Alzheimer's disease and other dementias, v 25(7), pp 547-555
01 Nov 2010
PMID: 20858652
url
https://europepmc.org/articles/pmc2976708View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Clinical Neurology Geriatrics & Gerontology Life Sciences & Biomedicine Neurosciences & Neurology Science & Technology
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.

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Web of Science research areas
Clinical Neurology
Geriatrics & Gerontology
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