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.
CAPSONI, Simona;
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.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
