Bin1 regulates synaptic endocytic trafficking compromised by Alzheimer’s genetic risk variants

Bin1 is an inhibitory presynaptic protein. The LOAD mutations may cause Bin1 loss of function, affecting inhibitory synapses. Losing inhibitory transmission may turn excitatory neurons hyperactive, accelerating the loss of excitatory synapses. In the future, we aim to dissect the underlying mechanisms by which Bin1 mutations interfere with Bin1's role in synaptic vesicle mechanisms at inhibitory presynaptic terminals.