TY - JOUR T1 - Synaptic Plasticity Defect Following Visual Deprivation in Alzheimer's Disease Model Transgenic Mice JF - The Journal of Neuroscience JO - J. Neurosci. SP - 8004 LP - 8011 DO - 10.1523/JNEUROSCI.5369-11.2012 VL - 32 IS - 23 AU - Christopher M. William AU - Mark L. Andermann AU - Glenn J. Goldey AU - Demetris K. Roumis AU - R. Clay Reid AU - Carla J. Shatz AU - Mark W. Albers AU - Matthew P. Frosch AU - Bradley T. Hyman Y1 - 2012/06/06 UR - http://www.jneurosci.org/content/32/23/8004.abstract N2 - 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 characterized, in vivo, developmental model of systems-level plasticity, ocular dominance plasticity. Following monocular visual deprivation during the critical period, mice that express mutant alleles of amyloid precursor protein (APPswe) and Presenilin1 (PS1dE9), as well as mice that express APPswe alone, lack ocular dominance plasticity in visual cortex. Defects in the spatial extent and magnitude of the plastic response are evident using two complementary approaches, Arc induction and optical imaging of intrinsic signals in awake mice. This defect in a classic paradigm of systems level synaptic plasticity shows that Aβ overexpression, even early in postnatal life, can perturb plasticity in cerebral cortex, and supports the idea that decreased synaptic plasticity due to elevated Aβ exposure contributes to cognitive impairment in AD. ER -