Thomas M. Piers

This study shows that Amyloid-β activates JNK signaling through WNT-5A/ROR2, reducing synapse formation in Alzheimer's disease.

This study shows microglia produce ABri peptide in FBD, contributing to amyloid plaques and neurodegeneration, and suggests ITM2B/BRI2 is involved in microglial disease responses.

This study investigates how metabolite supplementation affects metabolic and functional deficits in TREM2-mutant human iPSC-derived microglia, identifying distinct effects of citrate and succinate on mitochondrial function and phagocytosis.

The paper shows that Wnt-7a signaling from dendritic filopodia, combined with calcium signaling, is essential for synapse formation in cortical neurons.

The paper examines how TREM2 variants affect microglial exosomal proteomes and their functional impact on neurons.

The paper shows that the R47H TREM2 variant impairs microglial signaling and inflammasome activation, potentially contributing to Alzheimer's disease progression.

The paper identifies a genetic variant in OAS1 linked to increased Alzheimer's disease risk and severe COVID-19 outcomes, showing its role in microglial inflammation.

This study investigates how TREM2 influences microglial anti-inflammatory responses and shows that reduced TREM2 expression impairs anti-inflammatory gene expression and STAT6 levels.

This study shows that TREM2 loss-of-function variants in human iPSC-derived microglia impair metabolic switching and PPARγ/p38MAPK signaling, affecting β-Amyloid phagocytosis.