Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A framework to understand the variations of PSD-95 expression in brain aging and in Alzheimer's disease.

Ageing research reviews - 1 Nov 2014

Savioz Armand, Leuba Geneviève, Vallet Philippe G

Abstract excerpt

The postsynaptic density protein PSD-95 is a major element of synapses. PSD-95 is involved in aging, Alzheimer's disease (AD) and numerous psychiatric disorders. However, contradictory data about PSD-95 expression in aging and AD have been reported. Indeed in AD versus control brains PSD-95 varies according to regions, increasing in the frontal cortex, at least in a primary stage, and decreasing in the temporal...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Age Factors
Share to Aging
Share to Alzheimer Disease

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Disks Large Homolog 4 Protein

Share to Intracellular Signaling Peptides and Proteins

Share to Mice, Transgenic

Share to Models, Biological

Source

Identifiers

PMID: 25264360
DOI: 10.1016/j.arr.2014.09.004

Genes

PSD

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A framework to understand the variations of PSD-95 expression in brain aging and in Alzheimer's disease.PMID 25264360Read ↗

Postsynaptic degeneration as revealed by PSD-95 reduction occurs after advanced Aβ and tau pathology in transgenic mouse models of Alzheimer’s diseaseSemantic proximity Read ↗

Reduction in post-synaptic scaffolding PSD-95 and SAP-102 protein levels in the Alzheimer inferior temporal cortex is correlated with disease pathology.Semantic proximity Read ↗

Synaptic Compensation as a Probable Cause of Prolonged Mild Cognitive Impairment in Alzheimer’s Disease: Implications from a Transgenic Mouse Model of the DiseaseSemantic proximity Read ↗

Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses.Semantic proximity Read ↗

Oxidative stress and hippocampal synaptic protein levels in elderly cognitively intact individuals with Alzheimer's disease pathology.Semantic proximity Read ↗

Selective loss of synaptic proteins in Alzheimer's disease: evidence for an increased severity with APOE varepsilon4.Semantic proximity Read ↗

Reduced Expression of the Inhibitory Synapse Scaffolding Protein Gephyrin in Alzheimer's DiseaseSemantic proximity Read ↗

A mouse model of sporadic Alzheimer’s disease with elements of major depressionSemantic proximity Read ↗

Distinct domains within PSD-95 mediate synaptic incorporation, stabilization, and activity-dependent trafficking.Semantic proximity Read ↗

Phenotypic down-regulation of glutamate receptor subunit GluR1 in Alzheimer's disease.Semantic proximity Read ↗

PSD-93 Attenuates Amyloid-β-Mediated Cognitive Dysfunction by Promoting the Catabolism of Amyloid-β.Semantic proximity Read ↗

Reduced Spine Density in Specific Regions of CA1 Pyramidal Neurons in Two Transgenic Mouse Models of Alzheimer's DiseaseSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.