Swagata Ghatak

This study shows how neuronal lipid composition affects full-length tau assembly, mechanics, and membrane interactions, revealing distinct states of tau-membrane interaction based on lipid type and tau assembly state.

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

This study shows that lipid membrane interfaces drive α-synuclein condensation and fibrillation at low concentrations, revealing a mechanism for its propagation in neurodegeneration.

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 identifies TREK1 upregulation as a compensatory mechanism that delays cognitive decline in Alzheimer's Disease by counteracting Aβ42o-induced neuronal hyperexcitability.

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