Radhika Jagannathan, MD, PhD

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Radhika Jagannathan, MD, PhD is an instructor of neurology in the Division of Aging and Dementia and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain. She completed her undergraduate studies in biology at the Massachusetts Institute of Technology, followed by a dual-degree program at Washington University in St. Louis, where she attained both her medical degree and PhD in molecular cell biology. Dr. Jagannathan completed her internship and residency in neurology at NewYork-Presbyterian/Weill Cornell Medicine, serving as chief resident in her final year. During fellowship in behavioral neurology at NewYork-Presbyterian/Columbia University Irving Medical Center, Dr. Jagannathan worked in the Taub Institute laboratory of Dr. Ulrich Hengst, investigating how changes in transcription factor regulatory mechanisms can drive programmatic changes in gene expression and contribute to disease pathogenesis. Dr. Jagannathan specializes in patients with memory disorders in her Aging and Dementia practice, and also sees patients with Huntington’s disease through the multidisciplinary Huntington's Disease Society of America Center of Excellence at Columbia.

Academic Appointments

  • Postdoctoral Clinical Fellow in the Department of Neurology and Assistant in Clinical Neurology


  • Female

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710 West 168th Street
New York, NY 10032

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Credentials & Experience

Education & Training

  • Washington University in St. Louis School of Medicine
  • Internship: NewYork-Presbyterian Hospital/Weill Cornell Medical Center
  • Residency: NewYork-Presbyterian Hospital/Weill Cornell Medical Center


Dr. Jagannathan is interested in understanding the cell biologic mechanisms underlying neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. Specifically, she is interested in transcription factors, which are important cellular components that govern gene expression through protein-DNA interactions. Her work is focused on understanding how changes in transcription factor regulatory mechanisms can drive programmatic changes in gene expression and contribute to disease pathogenesis.