Beisha Tang

Small-molecule autophagosome-tethering compounds selectively lower mutant ataxin-3 through an LC3- and autophagy-dependent mechanism and improve disease-related phenotypes in preclinical models of SCA3.

This study identifies genetic associations between lysosomal genes and Parkinson's disease risk across diverse populations using GWAS and whole genome sequencing data.

This study identifies population-specific eQTLs in brain tissues from European, African American, and Asian ancestry individuals, revealing new schizophrenia risk genes and variants missed in European-only datasets.

This paper conducts a multi-ancestry genome-wide meta-analysis of Parkinson's disease, identifying 78 independent loci and 23 genes associated with PD risk.

The paper introduces SEAD, an Asian reference panel that improves rare variant imputation and GWAS analysis, identifying a novel association between SNTG1 and hip BMD.

The paper outlines the protocol for integrating genetic and clinical data from a global cohort of over 150,000 participants to study the genetic causes of sporadic Parkinson's disease.

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

The paper evaluates 24 computational methods for predicting non-coding variant function and pathogenicity across four benchmark datasets, finding varying performance across different variant types.

This study shows that deficiency in DAGLB, an endocannabinoid synthase, contributes to Parkinson's disease by impairing dopaminergic neuron function and motor learning, with potential therapeutic implications for 2-AG augmentation.

The paper presents genomic analyses of 10,376 Chinese individuals, identifying novel genetic variations and providing a reference haplotype map, along with an imputation server for improved accuracy.

This study identifies eQTL and sQTL in East Asian brains, finds convergence in transcriptional regulatory architecture with European populations, and links these to schizophrenia risk genes and pathways.

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

This study investigates mitochondrial DNA mutations in SCA3/MJD patients and finds higher mutation frequency but no significant copy number difference compared to healthy controls.