Synaptic plasticity defect following visual deprivation in Alzheimer's disease model transgenic mice

Amyloid-β (Aβ)-induced changes in synaptic function in experimental models of Alzheimer's disease (AD) suggest that Aβ generation and accumulation may affect fundamental mechanisms of synaptic plasticity. To test this hypothesis, we examined the effect of APP overexpression on a well characteri...

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Veröffentlicht in:	The Journal of neuroscience 2012-06, Vol.32 (23), p.8004-8011
Hauptverfasser:	William, Christopher M, Andermann, Mark L, Goldey, Glenn J, Roumis, Demetris K, Reid, R Clay, Shatz, Carla J, Albers, Mark W, Frosch, Matthew P, Hyman, Bradley T
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - genetics Alzheimer Disease - physiopathology Amyloid beta-Protein Precursor - genetics Animals Eye Enucleation Fluorescence Humans Image Processing, Computer-Assisted Immunohistochemistry In Situ Hybridization Mice Mice, Inbred C57BL Mice, Transgenic Neuronal Plasticity - physiology Neurons - physiology Photic Stimulation Polymerase Chain Reaction Presenilin-1 - genetics RNA, Messenger - biosynthesis RNA, Messenger - genetics Sensory Deprivation - physiology Synapses - physiology Vision, Ocular - physiology Visual Cortex - cytology Visual Cortex - physiology
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