Affiliations: [a] Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, Italy | [b] Neurotrophins and Neurodegenerative Diseases Unit, European Brain Research Institute, Rome, Italy
Correspondence:
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Correspondence to: Antonino Cattaneo, Laboratory of Biology BioSNS Scuola Normale Superiore, Piazza dei Cavalieri 7, 56126 Pisa, Italy. Tel.: +39 0503153198; Fax: +39 0503153220; E-mail: antonino.cattaneo@sns.it.
Note: [1] Current Affiliation: Centre for Nanotechnology Innovation, Pisa, Italy and Centre for Neuroscience and Cognitive Systems, Italian Institute of Technology, Italy.
Abstract: 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.
Keywords: 5XFAD, amyloid-β peptides, plasticity impairment, sensory deprivation, visual system
