Autosomal dominant forms of familial Alzheimer’s disease are linked to an aberrant processing of the amyloid-protein precursor, which results in an increased production of amyloid-(A) peptides that first form oligomers and eventually aggregate in the form of extracellular amyloid plaques in the brain. The accumulation of A peptides oligomers seems to correlate with alterations of synaptic transmission in experimental models of Alzheimer’s disease. Whether A 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.

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

MAYA VETENCOURT, JOSE FERNANDO;CARUCCI, NICOLA MARIA;CAPSONI, SIMONA;CATTANEO, ANTONINO
2014

Abstract

Autosomal dominant forms of familial Alzheimer’s disease are linked to an aberrant processing of the amyloid-protein precursor, which results in an increased production of amyloid-(A) peptides that first form oligomers and eventually aggregate in the form of extracellular amyloid plaques in the brain. The accumulation of A peptides oligomers seems to correlate with alterations of synaptic transmission in experimental models of Alzheimer’s disease. Whether A 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.
2014
5XFAD; amyloid-β peptides; plasticity impairment; sensory deprivation; visual system
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11384/39800
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