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Results In this study, we found that LPL-deficient mice exhibited increased latency to escape platform and increased mistake frequency. Decreased latency to platform in the stepdown passive avoidance test was observed, consistent with impaired learning and memory in these mice. Transmission electron microscopy revealed a significant decrease in the number of pre-synaptic vesicles in the hippocampus of LPL-deficient mice. The levels of the pre-synaptic marker synaptophysin were also reduced in the hippocampus while post-synaptic marker PSD-95 levels remained unchanged in LPL-deficient mice. LPL deficiency reduced the frequency of miniature excitatory postsynaptic currents (mEPSCs) and readily releasable pool (RRP) size. Then we demonstrated that these defects, which resulted from slower clathrin-mediated endocytosis and synaptic vesicle recycling, led to presynaptic dysfunction and synaptic plasticity impairment. Moreover, lipid assay revealed a lack of docosahexaenoic acid (DHA) and arachidonic acid (AA) in LPL deficient neurons. Meanwhile, exogenous DHA and AA partially rescued the defect of synaptic vesicle recycling in LPL deficient neurons. Conclusion

molecular neurodegeneration

Implication of lipid metabolism disturbance and Alzheimer’s disease: focus on the lipoprotein lipase plays an important role in learning and memory function