Zhenyu Yue

This study identifies AKAP11 as a critical autophagy receptor linking PKA kinase network regulation to synaptic transmission, with loss-of-function impacting pathways associated with bipolar disorder and schizophrenia.

This study identifies Senescent Astrocytic Deposits (SAD) as a mechanism linking astrocyte senescence to synaptic dysfunction and cognitive decline in aging brains.

This study investigates how the LRRK2-N2081D variant increases Crohn's disease risk by showing it causes more severe colitis and distinct RAB substrate phosphorylation compared to LRRK2-G2019S.

This study identifies cortical tension as a mechanical barrier that prevents premature neuronal differentiation during neurogenesis, showing that reducing it accelerates neuronal lineage commitment and differentiation.

This study identifies RAB12 as a LRRK2 substrate in mouse brains, shows its role in suppressing ciliogenesis and regulating centrosome homeostasis in astrocytes, and demonstrates that disrupting RAB12 mitigates PD-linked LRRK2 mutation effects.

This study shows that Rit2 loss in dopamine neurons causes PD-like symptoms in mice, with sex-specific differences in disease progression and response to treatment.

The paper uses integrated proteomics to identify autophagy targets and receptors in human neurons, revealing their role in degradation and neuronal activity regulation.

This study generates a large single-cell RNA sequencing dataset of the human substantia nigra in Parkinson's disease, identifies DA neuron subtypes, and reveals molecular changes associated with PD.

This study identifies a novel neuroprotective mechanism where microglia clear neuron-released α-synuclein via TLR4-NF-κB-p62 mediated selective autophagy, preventing neurodegeneration.

This study identifies molecular networks and key regulators in Alzheimer’s Disease using integrative genomics and experimental validation.

This study shows that CSF-1 signaling is essential for cerebellar microglia identity and function, and its disruption causes motor and social behavior defects.

This study shows that misfolded α-synuclein spreads from urogenital nerves to the brain, causing MSA-like symptoms through micturition reflex pathways.

This study shows that reduced SYNJ1 expression with age contributes to dopamine neuron vulnerability and Parkinson's disease pathogenesis in mice.