Joseph R. Herdy

This paper introduces an age-preserving neuronal iSpheroid platform that models human aging and Alzheimer's disease, revealing disease-associated metabolic changes and potential therapeutic targets.

This study shows that nuclear acetyl-CoA accumulation in Alzheimer's disease neurons causes RBP hyperacetylation and splicing shifts, which can be reversed by inhibiting ACLY.

This study identifies LINE-1 retrotransposons as drivers of neuronal senescence in Alzheimer's disease through cytoplasmic DNA sensing and the cGAS-STING pathway.

This paper identifies the PFKFB3-F2,6BP metabolic axis as a key driver of Alzheimer's disease by linking metabolic dysregulation to genomic stability and Tau proteostasis, showing that F2,6BP supplementation rescues AD phenotypes across multiple models.

This study identifies RUNX1 and YY1 as master transcription factors modulating neuronal fate and energy metabolism in Alzheimer's disease using patient-derived induced neurons and post-mortem brain data.

This study shows DNA damage in neurons leads to a senescent-like state similar to Alzheimer's disease, with distinct features from fibroblasts.