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.
|Titolo:||Amyloid plaque-independent deficit of early postnatal visual cortical plasticity in the 5xFAD transgenic model of Alzheimer's disease.|
|Data di pubblicazione:||2014|
|Parole Chiave:||5XFAD; amyloid-β peptides; plasticity impairment; sensory deprivation; visual system|
|Digital Object Identifier (DOI):||http://dx.doi.org/10.3233/JAD-140453|
|Appare nelle tipologie:||1.1 Articolo in rivista|