Dr. Abhi Iyer

Abhi Iyer

Assistant Professor of Psychiatry

Education & Training


  • Ph.D.: Indiana University Indianapolis, 2016
  • Ph.D.: Indiana University Indianapolis, 2016
  • M.S.: University of Mumbai, 2009
  • B.S.: University of Mumbai, 2007

Major Awards


  • Knight ADRC Developmental Project Award, 2026-2027
  • Knight ADRC REC Scholar, 2025-2027
  • CurePSP Pipeline and Pathway Grant, 2025-2027
  • George Bartzokis Travel Award, New Vision Research, 11th Annual Charleston Conferences on Alzheimer’s Disease, 2023
  • Hope Center for Neurological Disorders and the Washington University Institute of Clinical and Translational Sciences, Just-in-time (JIT) core usage award, 2022
  • Indiana University School of Medicine postdoctoral travel grant for the Society for Neuroscience meeting, 2017
  • Indiana University School of Medicine graduate student travel grant for the American Association of Immunologists meeting, 2014
  • Indiana University Simon Cancer Center Annual Cancer Research Day, Honorable Mention in Basic Science Category by Graduate Student, 2013
  • Junior Research Fellowship, Council of Scientific & Industrial Research, India, 2010

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Research Interests


My research focuses on uncovering the cellular mechanisms driving neurodegeneration, specifically challenging the traditional view that microglia act merely as a reactive “clean-up crew” responding to existing neuronal pathology. Using human induced pluripotent stem cell (iPSC) models of Frontotemporal Dementia associated with tau pathology (FTD-tau), my work investigates how genetic mutations drive intrinsic, cell-autonomous defects within microglia themselves. By employing human stem cell-derived microglia, my work has uncovered that MAPT mutations implicated in tauopathies directly impair critical microglial functions – including phagocytosis, metabolic homeostasis, and inflammatory signaling. Uncovering these cell-autonomous defects is essential for identifying early, cell-type-specific therapeutic targets capable of slowing or stopping neurodegeneration in FTD and related tauopathies.

Key Focus Areas:
Cell-Autonomous Microglial Defects: Investigating how tau mutations directly cause intrinsic immune dysfunction independent of neuronal pathology.
Human iPSC Modeling: Utilizing patient-derived stem cells to model human-specific, cell-type-specific mechanisms in vitro .
Early Targeted Therapies: Shifting the FTD-tau therapeutic paradigm to intervene before overt neurodegenerative damage takes hold.

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Recent Publications


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