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Amyloid plaque-independent deficit of early postnatal visual cortical plasticity in the 5XFAD transgenic model of Alzheimer's disease.

Authors
  • Maya-Vetencourt, José Fernando
  • Carucci, Nicola Maria
  • Capsoni, Simona
  • Cattaneo, Antonino
Type
Published Article
Journal
Journal of Alzheimer s Disease
Publisher
IOS Press
Publication Date
Jan 01, 2014
Volume
42
Issue
1
Pages
103–107
Identifiers
DOI: 10.3233/JAD-140453
PMID: 24844685
Source
Medline
Keywords
License
Unknown

Abstract

Autosomal dominant forms of familial Alzheimer's disease are linked to an aberrant processing of the amyloid-β protein precursor, which results in an increased production of amyloid-β (Aβ) peptides that first form oligomers and eventually aggregate in the form of extracellular amyloid plaques in the brain. The accumulation of Aβ peptides oligomers seems to correlate with alterations of synaptic transmission in experimental models of Alzheimer's disease. Whether Aβ aggregation disrupts synaptic function independently of amyloid plaques deposition still needs further research. Here we report an amyloid plaque-independent deficit of neuronal plasticity after short-term sensory deprivation in the visual system of 5XFAD mice.

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