Excessive synaptic loss is thought to be one of the earliest events in Alzheimer’s disease (AD). In our previous studies, we have shown that amyloid beta (Aβ), a peptide implicated in the pathogenesis of AD, is secreted in an activity-modulated manner. Furthermore, we found that secreted Aβ leads to loss of synaptic receptors (by endocytosis), synaptic depression and removal of dendritic spines, sites of excitatory synaptic transmission. We now wish to understand the following: Can synaptic loss seen in AD transgenic animals be rescued by block of synaptic receptor endocytosis?
Rescue of Synapses in AD Rodent Models
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