Vilas Menon, PhD

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Dr. Menon obtained his PhD in Applied Mathematics from Northwestern University, where he studied signal integration and information processing in neurons. Prior to joining Columbia, he spent several years as a staff scientist at the Allen Institute for Brain Science in Seattle, WA, and as a Fellow at the Howard Hughes Medical Institute’s Janelia Research Campus, developing new analytical methods for large-scale single-cell and bulk molecular data analysis. At Columbia, his lab applies state-of-the-art computational and experimental methods to generate and analyze large-scale molecular data in the context of neurological disease. In particular, his group investigates signatures of differential vulnerability and resistance at both the cell type and individual level in neurodegenerative diseases (including Alzheimer’s and Parkinson’s) and neuroimmune diseases (such as Multiple Sclerosis).

Academic Appointments

  • Assistant Professor of Neurological Sciences (in Neurology and the Taub Institute for Research on Alzheimer Disease and the Aging Brain)


  • Male


  • Selective vulnerability of cell types in neurological disease – It has long been known that disease-specific pathologies do not have uniform effects on all cell types in the brain. A major arm of our research is to systematically identify and investigate the differential impacts of pathology on cell types in the human brain. To achieve this, we combine single-cell and bulk methods with spatially-resolved molecular methods on post-mortem human brain tissue to develop integrative models evaluating cell type-specific dysregulation. We apply these approaches to multiple diseases, with a number of clinical and experimental collaborators at Columbia and beyond.
  • Individual resilience to pathology – In diseases such as Alzheimer’s, Parkinson’s, and Multiple Sclerosis, certain individuals exhibit minimal cognitive and/or motor symptoms despite having substantial disease-specific pathology in their brains (as identified post-mortem). This suggests that these rare individuals may have compensatory mechanisms allowing them to maintain regular function even in the presence of deleterious perturbations. Here, we apply a suite of computational and experimental profiling methods to characterize resilience-associated signatures, which are distinct from risk factors for these diseases.
  • Reproducibility in studies within and across diseases – The explosion of large-scale molecular profiling methods for genome-wide single-cell and spatial data generation has led to a wealth of published studies investigating post-mortem human brain tissue in a variety of diseases. A major area of our research is evaluating and prioritizing cell type-specific observations in various neurological diseases based on findings from multiple studies. This type of prioritization is key to identifying potentially robust targets for disease-specific therapeutics.


  • NIH R01 AG066831 Elucidating changes in astrocyte subpopulations associated with resistance to Alzheimer’s Disease pathology in multi-ethnic cohorts
  • NIH R01 AG057911 Identifying the molecular systems, networks, and key molecules that underlie cognitive resilience
  • NIH U01 AG061356 Multi-omic network-directed proteoform discovery, dissection and functional validation to prioritize novel AD therapeutic targets
  • Parkinson's Disease Foundation Differential neuronal susceptibility as an avenue toward disease-modifying therapy for Parkinson’s Disease
  • Chan-Zuckerberg Initiative CS-02018-191971 Creating and deploying a toolkit for human microglia in neurodegeneration
  • NIH R21AG064596 A transcriptomic atlas of immune cells in a model of synucleinopathy
  • NIH R01AG015819 Risk factors, pathology, and clinical expressions of AD
  • National MS Society RG-1901-33218 Endothelial Wnt signaling in CNS neo-angiogenesis and blood brain barrier in EAE/MS
  • NIH RM 1HG011014 Center for Integrated Cellular Analysis
  • NIH R01 AG067581 Microglia antigen presentation in the CNS of Alzheimer’s disease