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Bio

Aryeh Zolin, MD, PhD

2025 Leon Levy Scholar in Neuroscience

Weill Cornell Medicine, NewYork-Presbyterian/Weill Cornell Medical Center

Sub-disciplinary Category

Cellular & Molecular Neuroscience

Previous Positions

  • BA, Columbia University
  • PhD, The Rockefeller University (Dr. Vanessa Ruta)
  • MD, Weill Cornell Medical College

Bio

Dr. Aryeh Zolin is interested in understanding Parkinson’s disease and related neurodegenerative disorders. As an undergraduate at Columbia University, he investigated dopaminergic neuron development and degeneration in mouse models of Parkinson’s disease. He attended medical school at Weill Cornell Medicine and received his PhD at the Rockefeller University as part of the Tri-Institutional MD/PhD program. He earned his PhD in the laboratory of Vanessa Ruta studying dopaminergic pathways in the fruit fly brain. Dr. Zolin then pursued clinical training in Neurology at New York Presbyterian – Weill Cornell Medicine where he was the Resident Research Fellow at the Feil Family Brain and Mind Research Institute and the McGraw Fellow in Neurology Research. He is currently pursuing a Fellowship in Movement Disorders at Weill Cornell Medicine. As a Leon Levy Research Fellow he will be working in the laboratories of Jacqueline Burré and Manu Sharma at Weill Cornell studying the pathogenesis of Parkinson’s disease. 

Research Summary

Examining how the pathology that causes neurodegeneration in Parkinson’s Disease is transmitted between neurons and spreads through neural circuits.

Technical Overview

Parkinson’s disease (PD) is caused by misfolded alpha-synuclein (aSyn) aggregates that have prion-like properties: they are transmitted between neurons and act as seeds, triggering the aggregation of local aSyn. The pathology spreads through neural networks and there are no treatments to slow the disease’s progression. Dr. Zolin is developing a new model to study how misfolded aSyn is transmitted through neural circuits. Using an innovative combination of genetic, biochemical, and surgical approaches, he is seeding aSyn aggregation in distinct neural subpopulations. He is then applying novel 3D imaging methods to generate high-resolution brain maps to characterize and compare differences in the extent and distribution of aSyn aggregation when the pathology is initiated in different neuronal subsets. These experiments will explore how cellular properties, molecular composition, and connectivity patterns impacts a neuron’s propensity to spread aSyn pathology. In the future, this system will identify and assess the role of specific proteins in the propagation of aSyn pathology and test the efficacy of different therapeutic interventions. This work will help determine the mechanism underlying trans-neuronal propagation of aSyn misfolding and aggregation, significantly advancing our understanding of PD pathophysiology.