Stuart A. Lipton

AA-20 promotes lipophagy by activating lysosomal acid lipase and CDK5, reducing lipid droplet accumulation and improving neurodegeneration-associated phenotypes in cellular and organoid models.

The paper characterizes extracellular vesicles from Alzheimer's disease and wild-type cerebrocortical organoids, finding differences in size, membrane structure, and proteomic content.

The paper identifies S-nitrosylation of STING as a redox modification driving aberrant cGAS-STING signaling in Alzheimer's disease, contributing to neuroinflammation and synaptic loss.

This study uses human iPSC-derived cortical organoids to model familial Alzheimer's disease and shows that autophagy activators reduce pathological Tau and Aβ accumulation and rescue synaptic loss.

This study shows that S-nitrosylation of CRTC1 impairs CREB-dependent gene expression in Alzheimer's disease models, leading to synaptic dysfunction and suggesting a therapeutic target.

The paper introduces a method to detect boolean asymmetric relationships in gene expression data, identifying heterogeneity driven by asymmetric gene interactions and showing improved classifier performance.

Autism-like MEF2C+/- patient hiPSC models show miRNA-mediated overproduction of astrocytes and hyperactivity of neurons.

This study identifies a metabolic block in the TCA cycle in Alzheimer's disease neurons and shows that dimethyl succinate treatment rescues mitochondrial function and synapse loss.

The paper shows that manipulating the UPR pathway can restore brain function and reduce aging-related deficits.