Robert J. Vassar

This study shows neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD mice by lowering BACE1 and other proteins in these structures.

This study shows that influenza A infection accelerates the formation of disease-associated microglia in aging mice, with effects observed in white matter regions.

This study investigates whether ACE1 influences Aβ degradation or amyloid plaque accumulation in 5XFAD mice, finding no effect on amyloid burden or neuroinflammation.

The paper discovers that levetiracetam prevents Aβ42 production by modulating synaptic vesicle cycling, altering APP localization, and favoring non-amyloidogenic processing in Alzheimer's disease models.

The paper shows oligodendrocytes contribute to amyloid-β plaques in Alzheimer's disease, but neurons are required for plaque formation.

This study shows that oligodendrocytes produce amyloid beta in Alzheimer's Disease and that suppressing this production improves brain pathology and neuronal function.

This study shows that neuronal ACE1 knockout in mice causes hippocampal RAS dysregulation and vascular loss without affecting motor skills.

The paper uses single-cell transcriptomics to show Evf2 lncRNA guides Dlx5/6UCE to many enhancer-gene guidance sites, with subpopulation-specific effects and long-range gene regulation.

The paper isolates and analyzes amyloid fibrils from AD brains and models to identify proteins associated with fibril formation and toxicity, finding new proteins and validating their roles.

The paper identifies DISE, an RNA interference-mediated cell death mechanism, as correlated with neurotoxicity in Alzheimer's disease and aging, showing shifts in 6mer seed toxicity in different models.

This study shows that astrocyte senescence in Alzheimer’s disease mice is driven by TGF-β1 and contributes to neurotoxicity.