
About
Avi Samelson is an Assistant Professor in the Department of Neurology at the David Geffen School of Medicine, University of California, Los Angeles, where he leads an independent research program focused on protein folding, misfolding, and aggregation mechanisms in neurodegenerative diseases. His work bridges biophysics, neuroscience, and genetic engineering to identify therapeutic targets for conditions like Alzheimer's disease.
Dr. Samelson completed his doctoral training in Susan Marqusee’s laboratory at UC Berkeley, developing novel technologies to study protein folding during translation in physiological contexts. He then pursued postdoctoral research with Martin Kampmann at UCSF, establishing CRISPR-based screening platforms in iPSC-derived neurons to investigate tau aggregation in neurodegenerative disorders.
His research employs integrated biophysical, biochemical, and systems genetics approaches to characterize protein aggregation trajectories—the conformational states proteins traverse en route to aggregation—and identify cellular mechanisms controlling these processes. Key focus areas include:
- Impact of translation dynamics on protein folding stability and kinetics
- Cell-type-specific regulation of tau aggregation in Alzheimer's disease
- Role of oxidative stress in tau cleavage fragment accumulation
- Discovery of genetic modifiers like the tau E3 ubiquitin ligase CRL5SOCS4
- Development of disease-relevant neuronal models for mechanistic discovery
- Therapeutic target identification for protein aggregation diseases
Dr. Samelson's laboratory leverages cutting-edge techniques including nascent chain probing, CRISPR screening, and iPSC-derived neuron models to uncover fundamental principles of protein homeostasis and develop novel interventions for neurodegeneration.
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