Brian J. Wainger

The paper identifies cis-regulatory elements for targeted gene delivery to nociceptors using multi-omic profiling and develops a sequence-based model to design synthetic enhancers.

The paper shows statins and mevalonate pathway inhibition increase STMN2 and ATF3, promoting neuronal regeneration in neurodegenerative disease.

The paper identifies RIG-I-mediated innate immune activation in FUS-ALS spinal motor neurons due to mitochondrial dsRNA accumulation, which can be targeted by JAK-STAT inhibition, offering potential biomarker-driven treatment options.

The paper identifies a specific subtype of injured C-fibre nociceptors in neuromas that drive chronic spontaneous neuropathic pain in mice.

This study identifies interleukin-1 as the key cytokine mediating rapid adaptive increases in heat and mechanical sensitivity in skin following capsaicin exposure.

The paper shows that reduced Kv8.1 expression in ALS motor neurons with SOD1(A4V) and C9orf72 mutations increases vulnerability to cell death by affecting metabolism and transport pathways.

This study identifies GSDME as a mediator of mitochondrial damage and axon loss in neurodegenerative diseases, showing its role in ALS and FTD models.

The paper identifies and characterizes a reference iPSC line, KOLF2.1J, for standardized use in collaborative studies across multiple differentiation protocols and assays.

This study evaluates human-derived anti-poly-GA antibodies in cellular and animal models of C9ORF72 disease, showing mixed effects on poly-GA levels and disease progression.

The paper shows iPSC-derived spinal motor neurons with familial ALS mutations capture gene expression changes seen in postmortem sporadic ALS motor neurons, particularly in TDP-43-related splicing dysregulation.

The paper introduces APPOINT, a platform for high-throughput physiological profiling of individual neurons, identifying subtypes and mechanisms of activation and drug responses.

The paper develops a cultured sensorimotor organoid model that forms functional neuromuscular junctions and uses it to study ALS subgroups.

This study identifies the causal mechanism of X-linked Dystonia-Parkinsonism (XDP) by integrating genome and transcriptome assembly, revealing a SVA insertion causing intron retention and TAF1 dysfunction.