Amyloid plaque-independent deficit of early postnatal visual cortical plasticity in the 5XFAD transgenic model of Alzheimer's disease.
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.
Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, Italy.
José Fernando
JF
Maya-Vetencourt
Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, Italy.
Nicola Maria
NM
Carucci
Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, Italy.
Simona
S
Capsoni
Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, Italy Neurotrophins and Neurodegenerative Diseases Unit, European Brain Research Institute, Rome, Italy.
Antonino
A
Cattaneo
D000544:Alzheimer Disease / Q000503:physiopathology*; D000818:Animals; D004195:Disease Models, Animal; D051379:Mice; D008822:Mice, Transgenic; D009473:Neuronal Plasticity / Q000502:physiology*; D058225:Plaque, Amyloid / Q000503:physiopathology; D012683:Sensory Deprivation / Q000502:physiology*; D013997:Time Factors; D015348:Vision, Binocular / Q000502:physiology; D015349:Vision, Monocular / Q000502:physiology; D014793:Visual Cortex / Q000503:physiopathology*; D014796:Visual Perception / Q000502:physiology*
5XFAD; amyloid-β peptides; plasticity impairment; sensory deprivation; visual system