George S. Bloom

The paper shows that mitochondrial NADK2-dependent NADPH synthesis mediates Tau oligomer uptake in neurons via LRP1, creating a cycle that exacerbates TauO toxicity.

This paper introduces using Benzonase to generate ribosome footprints for Ribo-seq, simplifying the protocol and reducing time, cost, and bias.

LiFE, a circadian intervention combining light, food, and exercise, improves sleep, glycemic control, and memory in mice.

The paper shows that mitochondrial response to nutrients is disrupted early in the cortex of APPSAA mice before symptoms appear, suggesting it as a presymptomatic event in Alzheimer's disease.

This study investigates how extracellular tau oligomers cause structural and functional damage to neuronal nuclei in tauopathies, showing increased invaginations and altered gene expression.

The paper identifies SOD1 as a mediator of lysosome-to-mitochondria communication and shows its dysregulation by amyloid-β oligomers in Alzheimer's disease.

This study investigates the localization, induction, and cellular effects of tau-phospho-threonine 217 in brain and cultured neurons, finding increased levels in AD progression and reduced tau affinity for microtubules.

The paper analyzes transcriptional and translational regulation in Alzheimer's disease model mice to identify gene expression changes and their functional implications.

This study accelerates and standardizes the maturation of iPSC-derived neurons by optimizing extracellular cues, resulting in synchronized neurogenesis and earlier calretinin expression.