Yasir H. Qureshi, MD

Assistant Professor of Neurological Sciences (in Neurology) at the Columbia University Medical Center

Overview

I am an Assistant Professor of Neurological Sciences at Columbia University Vagelos College of Physicians and Surgeons (VP&S) and a physician-scientist focused on the molecular mechanisms that drive neurodegenerative disease, with particular emphasis on endolysosomal dysfunction in neurons and glia. My research combines mechanistic neuroscience with translational approaches, including genetic engineering, gene therapy, small molecules, peptide-based therapeutics, and in vivo and cell-based disease models, to better understand and treat disorders such as Alzheimer’s disease, Parkinson’s disease, and frontotemporal dementia. A central theme of my work is retromer-dependent endosomal trafficking, which I have studied in relation to neuronal dysfunction, synaptic receptor trafficking, glial activation, and disease-associated protein processing. Through this program, I aim to define disease mechanisms with biological precision and advance therapeutic strategies that restore cellular trafficking, reduce pathological protein accumulation, and modulate neuroinflammation. My research is informed by clinical training and sustained collaboration across academic and industry settings, and I am committed to translating laboratory discoveries into meaningful therapeutic advances for patients with neurodegenerative disease.

Academic Appointments

Assistant Professor of Neurological Sciences (in Neurology) at the Columbia University Medical Center

Languages

English
Hindi
Urdu

Credentials & Experience

Education & Training

MD, 2008 University of Health Sciences, Lahore Pakistan
Fellowship: 2019 Columbia University Vagelos College of Physicians and Surgeons (VP&S), NY

Honors & Awards

Invited lecture: The Royal Society. 6-9 Carlton House Terrace, London, United Kingdom. The Royal Society is a Fellowship of many of the world's most eminent scientists and is the oldest scientific academy in continuous existence.
Gold medal, graduating Summa Cum Laude in med school human physiology.

Research

My research focuses on the molecular basis of neurodegeneration, using gene therapy and translational models to restore endolysosomal function and reduce disease pathology.

My research examines the molecular mechanisms that underlie neurodegenerative disease, with a focus on endolysosomal dysfunction, retromer biology, and the resulting effects on neuronal and glial health. Using a translational approach that integrates mouse models, iPSC-based systems, viral gene delivery, and biochemical and histopathological analyses, I study how trafficking defects contribute to Alzheimer’s disease and related disorders. A major goal of my work is to identify therapeutic strategies that restore endosomal and lysosomal function, reduce pathological protein accumulation, and modulate neuroinflammation. This research builds on a strong foundation in neuroscience, gene therapy, and clinical-translational investigation, with the aim of advancing more effective treatments for patients with neurodegenerative disease.

Selected Publications

1. Yasir H. Qureshi, Charles A. Williams, Istvan Hajdu, Suvarnambiga Kannan, Ananya Govindarajan, Barbara Végh, Gregory A. Petsko, Jessica E. Young, Péter Závodszky, Scott A. Small RhoGEF12 regulates endosomal SORL1-retromer and its inhibition is therapeutic in human neuronal models of Alzheimer’s disease.

2. Qureshi, Y.H., Berman DE, Marsh SE, Klein RL, Patel VM, Simoes S, Kannan S, Petsko GA, Stevens B, Small SA. The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer’s Disease. Cell reports. 2022;38. doi: 10.1016/j.celrep.2021.110262.

3. Simoes S, Guo J, Buitrago L, Qureshi, Y.H., Feng X, Kothiya M, Cortes E, Patel V, Kannan S, Kim YH, Chang KT, Hussaini SA, Moreno H, Di Paolo G, Andersen OM, Small SA. Alzheimer's vulnerable brain region relies on a distinct retromer core dedicated to endosomal recycling. Cell Rep. 2021 Dec 28;37(13):110182. doi: 10.1016/j.celrep.2021.110182. PubMed PMID: 34965419; PubMed Central PMCID: PMC8792909.

4. Qureshi, Y.H., Baez, P., and Reitz, C. (2020). Endosomal Trafficking in Alzheimer's disease, Parkinson's Disease and Neuronal Ceroid Lipofuscinosis. Molecular and cellular biology.

5. Qureshi, Y.H., Patel, V.M., Kannan, S., Waksal, S.D., Petsko, G.A., and Small, S.A. Retromer Combinatorials for Gene-Therapy Across a Spectrum of Neurological Diseases. BioRxiv 2020.

6. Simoes S, Neufeld JL, Triana-Baltzer G, Moughadam S, Chen EI, Kothiya M, Qureshi, Y.H., Patel V, Honig LS, Kolb H, Small SA. Tau and other proteins found in Alzheimer's disease spinal fluid are linked to retromer-mediated endosomal traffic in mice and humans. Science translational medicine. 2020;12(571). Epub 2020/11/27. doi: 10.1126/scitranslmed.aba6334. PubMed PMID: 33239387; PMCID: PMC7901670.

7. Qureshi, Y.H., Patel, V.M., Berman, D.E., Kothiya, M.J., Neufeld, J.L., Vardarajan, B., Tang, M., Reyes-Dumeyer, D., Lantigua, R., Medrano, M., et al. (2018). An Alzheimer's linked loss-of-function CLN5 variant impairs Cathepsin D maturation consistent with a retromer trafficking defect. Molecular and cellular biology.

8. Aubry S, Shin W, Crary JF, Lefort R, Qureshi, Y.H., Lefebvre C, Califano A, Shelanski ML. Assembly and Interrogation of Alzheimer’s disease genetic networks reveal novel regulators of progression. PLoS One. 2015 Mar 17;10(3):e0120352. doi: 10.1371/journal.pone.0120352. eCollection 2015. PMID: 25781952.

For a complete list of publications, please visit PubMed.gov