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J Alzheimers Dis. 2014;42(1):103-7. doi: 10.3233/JAD-140453.

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

Author information

1
Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, Italy.
2
Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, Italy Neurotrophins and Neurodegenerative Diseases Unit, European Brain Research Institute, Rome, Italy.

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.

KEYWORDS:

5XFAD; amyloid-β peptides; plasticity impairment; sensory deprivation; visual system

PMID:
24844685
DOI:
10.3233/JAD-140453
[Indexed for MEDLINE]

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