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.
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