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Amyloid plaque-independent deficit of early postnatal visual cortical plasticity in the 5XFAD transgenic model of Alzheimer's disease.
- Source :
-
Journal of Alzheimer's disease : JAD [J Alzheimers Dis] 2014; Vol. 42 (1), pp. 103-7. - Publication Year :
- 2014
-
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.
- Subjects :
- Animals
Disease Models, Animal
Mice
Mice, Transgenic
Plaque, Amyloid physiopathology
Time Factors
Vision, Binocular physiology
Vision, Monocular physiology
Alzheimer Disease physiopathology
Neuronal Plasticity physiology
Sensory Deprivation physiology
Visual Cortex physiopathology
Visual Perception physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1875-8908
- Volume :
- 42
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of Alzheimer's disease : JAD
- Publication Type :
- Academic Journal
- Accession number :
- 24844685
- Full Text :
- https://doi.org/10.3233/JAD-140453