Synaptic Dysfuction in Alzheimer’s Disease

Work by numerous labs has demonstrated that all members of the NgR family bind the Amyloid Precursor Proteins (APP), a gene mutated in Alzheimer’s disease. A proteolytic product of APP, ABeta, is likely a causal agent in the synaptic dynsfunction and learning and memory deficits underlying AD. How ABeta mediates synaptic loss is unclear. We propose that the NgR family may contribute to the synaptic deficits characterizing AD and aim to test this hypothesis by use of in vitro and in vivo models of AD (Fig. 4- NgR model).