Cell Sub-journal: Bin1 protein, the second leading risk factor for late-onsis AD, is also the key to the integration of spatial memory in the brain!

Bin1 (bridging integrator 1) is a member of the bar protein family. Genome wide studies have shown that Bin1 is also an important factor in the pathogenesis of late-onset Alzheimer's disease (AD).at present, about 40% of AD patients have mutations in Bin1 gene, but little is known about the role of Bin1 in the brain.recently led the research by the Gopal Thinakaran doctor of the USF Health University in Florida, and the researchers at University of Chicago, and found that BIN1 plays a non redundant role in presynaptic regulation. The loss of neurons in neurons can lead to impaired integration of spatial memory in the brain.the research results were published in the journal Cell reports.DOI:10.1016/j.celrep.2020.02.026 In order to explore the function of Bin1 protein, the researchers first constructed a Bin1 deficient Bin1 CKO mouse model, and carried out experiments from the behavioral and electrophysiological aspects. It was found that the loss of Bin1 expression in neurons would damage the consolidation of spatial memory, especially the release level of presynaptic vesicles, thus reducing synaptic transmission.then, using super-resolution microscopy and immunoelectron microscopy, the researchers found that Bin1 was located in the presynaptic site of excitatory synapses. Meanwhile, the recording results showed that the synaptic density decreased, the presynaptic protein aggregation and the distribution of neurotransmitter vesicles changed in bin1cko mice.neuronal Bin1 regulates the release of presynaptic neurotransmitters. To sum up, this study emphasizes that: 1) the loss of Bin1 in neurons may damage the spatial memory integration function of the brain; 2) neuronal Bin1 regulates the release of presynaptic neurotransmitters The excitatory synaptic transmission in cKO mice is defective; 3) BIN1 can regulate the release of presynaptic vesicles in hippocampal excitatory synapses; 4) emphasizes the non redundant role of BIN1 in presynaptic regulation.the researchers concluded that these important findings provide important insights into the basic function of Bin1 in synaptic physiology of Alzheimer's disease.end reference: [1] Bin1 defect impacts brain cell communication, memory consolidation [2] neural Bin1 regulations presynaptic neurotransmitter release and memory consolidation