Vilas Menon, PhD
- Associate Professor of Neurological Sciences (in Neurology and the Taub Institute for Research on Alzheimer Disease and the Aging Brain)
Overview
The Menon lab 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). The lab uses a combination of high-throughput molecular data generation, machine learning, bioinformatics, and computational biology approaches to investigate cell type-specific and spatial signatures associated with hallmarks of disease and resilience. This includes a combination of single-cell and spatial ‘omics techniques applied to human brain tissue as well as in vitro and in vivo model systems. Dr. Menon obtained his PhD in Applied Mathematics from Northwestern University and 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.
Academic Appointments
- Associate Professor of Neurological Sciences (in Neurology and the Taub Institute for Research on Alzheimer Disease and the Aging Brain)
Gender
- Male
Research
- 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.
Grants
- Protein and Lipid Homeostasis in the Aging Brain (Simons Foundation)
- Defining the effect of Alzheimer pathologies on the aged brain in 3 dimensions (NIH U19AG07486)
- Identifying cell type-specific autonomous and nonautonomous interactions in AD (NIH R01AG072167)
- AMP AD 2.0: Building a Multi-Ethnic, Single-Cell Molecular and Epigenetic Atlas of AD (FNIH)
- A Multi-Scale Atlas of Senescence in Diverse Tissue Types (NIH U54AG076040)
- Elucidating changes in astrocyte subpopulations associated with resistance to Alzheimer’s Disease pathology in multi-ethnic cohorts (NIH R01AG066831)
- Differential neuronal susceptibility as an avenue toward disease-modifying therapy for Parkinson’s Disease (Parkinson’s Disease Foundation)
- Creating and deploying a toolkit for human microglia in neurodegeneration (Chan Zuckerberg Initiative CS-0218-191971)