Ka Wan Li

The paper examines TMEM106B haplotypes and their associations with tau and TDP-43 pathologies in aging brains using integrated multi-omics data.

The paper identifies three neuron-specific schizophrenia protein networks enriched for genetic and transcriptional perturbations and validates their disruption in 22q11.2 deletion carriers.

This study shows Rab10 maintains Ca2+ homeostasis and protein synthesis to regulate neuropeptide release via DCVs in mouse hippocampal neurons.

The paper shows that GVB-positive neurons are protected against tau-induced protein synthesis impairment and neurodegeneration.

This study identifies type I TARPs as regulators of Kv7.2 potassium channels and shows their role in modulating neuronal excitability and seizure susceptibility.

The paper identifies a protein-protein interaction network in human excitatory neurons for 13 ASD risk genes, revealing novel interactions and convergent mechanisms contributing to autism spectrum disorders.

This study identifies ATXN3's role in regulating neuronal mRNA splicing and Tau isoform ratio through deubiquitylation of splicing factors, linking it to SCA3 pathology.

The paper identifies excessive ribosomal protein translation as a key factor in Fragile X Syndrome by showing its role in disrupting synaptic protein translation and LTD.

This study shows that β-amyloid oligomers cause synaptic depression by removing GluA3-containing AMPARs from synapses, requiring PDZ protein interaction.

This study identifies SNX4 as a novel synaptic protein through localization and functional analysis in neurons.

This study shows that Gpr158 deficiency in mice leads to impaired spatial memory and altered CA1 neuronal excitability and dendritic structure.

This study shows that CYFIP1 haploinsufficiency in mice causes reduced brain functional connectivity and white matter defects, linking it to neuropsychiatric disorders like Autism and Schizophrenia.