Nandi Lab
Nandi Lab
Howard University
College of Medicine
Microglia are the principal immune cell type of the central nervous system (CNS) and constitute ~90% of the myeloid compartment of the CNS. These cells are derived from embryonic yolk sac progenitors during the first wave of hematopoiesis and invade the brain parenchyma, where they proliferate and differentiate into mature microglia. Microglia survey the CNS environment, contribute to normal neurophysiological processes and play critical roles in the maintenance of the immune environment of the CNS. An altered microglial activity is often associated with an abnormal brain function. How these altered microglial functions and specific inflammatory pathways regulated by microglia contribute to the various CNS disorders remain largely unknown.
Our lab investigates the critical roles of microglia in brain health and disease, focusing on functional recovery and neural circuit remodeling. We previously explored the role of Iba1 (Ionized calcium-binding adapter protein 1), an actin-binding, pro-inflammatory protein widely recognized as a "microglial marker". Our study revealed that while Iba1 is essential for microglial structure and function, its absence leads to significant impairments in synaptic development and behavior. These findings highlight Iba1’s previously unrecognized role in maintaining microglial health and underscore the potential of targeting microglial pathways as a therapeutic strategy for neurodevelopmental, neuropsychiatric, and neurodegenerative disorders.
Sayan Nandi, Ph.D.
Principal Investigator
Assistant Professor
Department of Anatomy
Howard University College of Medicine
Location:
520 W Street NW
Mudd Bldg., Rm. 430
Washington, DC 20059
Office Phone: 202-806-6365
Email: sayan.nandi@howard.edu
Our Research
Neural Circuit Remodeling
Microglia, the resident immune cells of the brain, play a pivotal role in shaping neural circuits. These dynamic cells actively interact with neurons, forming and also removing excess synapses during development and maintaining synaptic integrity in adulthood. Our lab investigates how microglia contribute to neural circuit remodeling in both healthy and diseased states. Using advanced imaging techniques and molecular tools, we study the mechanisms by which microglia interact with neurons to regulate synaptic pruning, plasticity, and connectivity. Understanding these processes can provide insights into neurodevelopmental and neuropsychiatric disorders such as autism and schizophrenia and age-related cognitive decline, where microglial dysfunction may disrupt normal neural circuit dynamics.
Neural Injury and Recovery
In the aftermath of neural injury, microglia are among the first responders, initiating the brain’s repair mechanisms. Our research explores the dual role of microglia in neural recovery—promoting repair by clearing debris and modulating inflammation, while also potentially exacerbating damage if improperly activated. Through mouse models such as stroke, we investigate how microglia influence synaptic regeneration and functional recovery. By identifying pathways that enhance the beneficial effects of microglia and mitigate their harmful responses, we aim to uncover therapeutic targets for improving outcomes after neural injury.
Techniques
Cell Culture
Molecular Biology
Super-Resolution Microscopy
Biochemical and Immunological
Flow Cytometry
Mouse Genetic and Disease Models
Behavior
Electrophysiology
In Vivo manipulation
Research Support
HBMC/CZI Partnership in Genomics
News
Current Members
Alumni
Junia Lara deDeus, PhD
Postdoctoral fellow
Gaia Ressa, MD
Postdoctoral fellow
Evan Woo, BS
Undergraduate student (Laboratory Intern)
(Joint with Nicholas Sibinga, Einstein)
Collaborators
Nicholas E.S. Sibinga, M.D.
Professor, Department of Medicine (Cardiology)
Professor, Department of Developmental & Molecular Biology
Charles and Tamara Krasne Faculty Scholar in Cardiovascular Research
Albert Einstein College of Medicine
Selected Publications
1. de Deus J.L., Faborode, O.S., Nandi, S. (2024). Synaptic pruning by microglia: Lessons from genetic studies in mice. Developmental Neuroscience. Sep 12:1-21. PMID: 39265565 DOI: 10.1159/000541379
2. Chinnasamy, P., Casimiro, I., Riascos-Bernal, D.F., Venkatesh, S., Parikh, D., Maira, A., Srinivasan, A., Zheng, W., Tarabra, E., Zong, H., Jayakumar, S., Jeganathan, V., Pradan K., Aleman, J.O., Singh, R., Nandi, S., Pessin, J.E., Sibinga, N.E.S. (2023) Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1. Nature Communications. 14(1):38. PMID: 36596796 PMCID: PMC9810600
3. Lituma, P.J., Woo, E., O’Hara, B.F., Castillo, P.E., Sibinga, N.E.S., Nandi, S. (2021). Altered synaptic connectivity and brain function in mice lacking microglial adapter protein Iba1. Proceedings of the National Academy of Sciences. 118 (46) e2115539118 PMID: 34764226
4. Nandi, S., Mioce, M., Yeung, Y.G., Nieves, E., Tesfa, L., Lin, H., Hsu, A.W., Halenbeck, R., Cheng, H.Y., Gokhan, S., Mehler, M.F., Stanley, E.R. (2013). Receptor-type protein tyrosine phosphatase zeta is a functional receptor for interleukin-34. The Journal of Biological Chemistry. 288(30):21972-86. PMID: 23744080 PMCID: PMC3724651
5. Nandi, S., Gokhan, S., Dai, X.M., Wei, S., Enikolopov, G., Lin, H., Mehler, M.F., Stanley, E.R. (2012). The CSF-1 receptor ligands IL-34 and CSF-1 exhibit distinct developmental brain expression patterns and regulate neural progenitor cell maintenance and maturation. Developmental Biology. 367(2):100-13. PMID: 22542597 PMCID: PMC3388946
6. Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M.F., Conway, S.J., Ng, L.G., Stanley, E.R., Samokhvalov, I.M., Merad, M. (2010). Fate mapping analysis reveals that adult microglia derive from primitive macrophages. Science. 330(6005):841-5. PMID: 20966214 PMCID: PMC3719181
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