Beta Amyloid-Induced Synaptic Plasticity Imbalance and Neurogranin
While the application of amyloid beta (a precursor of AD) decreases neurogranin levels and suppresses synaptic transmission, increasing neurogranin in hippocampal neurons was able to reverse the beta amyloid-induced depression in synaptic transmission. We are proposing to understand the mechanism by which neurogranin is capable of such reversal of synaptic function and to explore the possibility that neurogranin may be reversing the synaptic plasticity imbalance. Success of this proposal can open the door for new therapeutic intervention for AD.
Previous studies have found that the Alzheimer's disease beta‐amyloid protein negatively influences brain cells (neurons) and results in a communication breakdown by causing a loss of “plasticity” at the synapses (the place where neurons meet), leading to learning and memory loss. In a previous study, Dr. Nashaat Gerges and colleagues have shown that increasing neurogranin enhances the ability of the synapses to communicate. In this project, they will explore the possibility that neurogranin may reverse the negative effect of beta amyloid on synaptic plasticity. They will use a special technique that grows neurons in a dish, giving easy access for treatments and analysis of results. If successful, this could lead to future therapies for individuals with Alzheimer's disease.