Zachary T. McEachin

This study uses human spinal cord organoids to model C9orf72 ALS, identifying early RNA splicing dysregulation and RBP network dysfunction as key features of the disease.

This study identifies TDP-43 dysfunction as a cause of cryptic circular RNA formation in ALS/FTD, showing their association with disease-relevant protein loss and potential as biomarkers.

This study identifies molecular subtypes based on cryptic exon burden in hippocampal tissue, revealing proteomic changes linked to TDP-43 pathology in LATE and Alzheimer's disease.

The paper identifies proteomic differences in cerebrospinal fluid between sporadic and familial ALS subtypes using network analysis and validates biomarkers across neurodegenerative diseases.

This study identifies TDP-43-driven splicing dysregulation as a common mechanism in ALS, FTD, and Alzheimer's disease, linking them through mis-spliced mRNAs like APP.

The paper identifies cell type-specific molecular changes in the prefrontal cortex of C9orf72 ALS/FTD patients correlated with pTDP-43 levels.

This study uses spatial proteomics to identify subregion-dependent protein changes in dementia variants, revealing disease-specific patterns in cortical layers and white matter.

This study uses cross-species scRNA-seq to show that the 3q29 deletion causes mitochondrial dysfunction in both human cortical organoids and mouse models, suggesting a conserved metabolic disruption in schizophrenia.

This study identifies TBK1 as a tau-interacting kinase that enhances neurodegeneration in tauopathies through increased tau phosphorylation.