Hu Wang

This study investigates the effects of PLCγ2 deficiency in mice, showing impaired immune tolerance, myelin homeostasis disruption, and enhanced oxidative metabolism in the brain.

This study uses single-nucleus RNA-sequencing to compare transcriptional changes in male and female mouse skeletal muscle during exercise and TFEB overexpression, revealing sex-specific metabolic adaptation mechanisms.

This study shows that APOE genotype affects neurovascular vulnerability in human forebrain organoids under viral stress, with APOE2/2 and APOE4/4 showing distinct inflammatory and vascular responses.

This study shows that MTCH2 deletion increases energy demand and metabolic imbalance in cells, which inhibits adipocyte differentiation.

This study identifies Lag3 as a neuronal receptor for Tau preformed fibrils, essential for their uptake, propagation, and transmission in Tauopathies.

This study investigates the effects of PLCγ2 deficiency in mouse brains using multi-omics approaches, revealing sex-specific changes in lipid and gene expression that may link to Alzheimer's disease and aging.

This study shows that deleting cGAS in microglia reduces amyloid-β plaque formation and cognitive impairment in Alzheimer's disease models.

This study shows that defects in mitochondrial biogenesis, not mitophagy, are the primary cause of mitochondrial alterations in PINK1-deficient human dopamine neurons.

This study shows that CNS sulfatide deficiency causes sex-dependent metabolic changes in aging, with females showing more severe metabolic disruption than males.

This study identifies that pathological α-synuclein destabilizes the TSC1-TSC2 complex, activates mTORC1, and enhances protein translation, contributing to neurodegeneration in Parkinson's disease.

The paper demonstrates the production of offspring from oocytes derived from mouse spermatogonial stem cells through chromatin reorganization and identifies key factors involved in germline stem cell conversion.