Michael A. Deture

This study shows TAF15 forms amyloid fibrils and propagates prion-like between cells, identifying specific motifs that drive its aggregation in vitro and in cells.

The paper decouples TDP-43 and Tau pathology in Alzheimer's disease by analyzing transcriptomic profiles and identifies subtype-specific transcriptional signatures.

The paper identifies TMEM106B fibril accumulation as a shared mechanism in neurodegeneration linked to genetic variants in TMEM106B and GRN.

The paper identifies epigenetic changes in Alzheimer's disease brains linked to tau pathology, highlighting oligodendrocyte gene perturbations as a potential common mechanism across tauopathies.

The paper characterizes ANXA11 proteinopathy in FTLD-PLS and MND-TDP cases, showing it is common in FTLD-PLS but not linked to pathogenic ANXA11 variants or TDP type C.

This paper develops and characterizes novel phospho-ubiquitin antibodies to detect low levels of p-S65-Ub, a marker of mitochondrial damage, in cells and tissues.

The paper creates a human iPSC model of 4R tauopathy and identifies genetic modifiers of Tau propagation using CRISPRi screening.

The paper creates a single-cell atlas of the human primary motor cortex in ALS and FTLD, identifying transcriptional changes and molecular similarities between Betz cells and VENs.

The paper identifies six genetic loci associated with Alzheimer's disease in Hispanics, showing both genetic and epigenetic risks, with some downstream effects on mRNA expression being ethnicity-specific.

This study performs a genome-wide association study of brain biochemical phenotypes in Alzheimer's patients, identifying novel genetic loci and highlighting distinct genetic architectures for AD-related proteins.

This study shows that reducing Csf3 in Csf1r+/- mice improves anxiety, motor coordination, and social interaction but not cognitive deficits, and reduces microglial activation in the cerebellum.

The paper identifies TMEM106B, not TDP-43, as the protein composing amyloid fibrils in FTLD-TDP using cryo-EM.

The paper identifies SERPINA5 as a novel tau binding partner in Alzheimer's disease by analyzing hippocampal gene expression and neurofibrillary tangles.

This study identifies R47H-TREM2 mutation-induced proinflammatory microglial states in human AD and tauopathy mice, showing Akt pathway involvement and potential therapeutic targets.

This study shows that reducing CSF-2 in Csf1r+/- mice rescues behavioral and histopathological deficits in ALSP by preventing microgliosis and transcriptomic changes, suggesting CSF-2 as a therapeutic target.