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Poulomi completed doctoral degree at Manipal University, India (2012–2017). Poulomi’s PhD work focused on elucidating the molecular mechanisms underlying Epithelial-to-Mesenchymal Transition (EMT) during neural crest cell formation and cancer metastasis (Banerjee et al., Stem Cells, 2016; Banerjee et al., Journal of Molecular Medicine, 2017).

During her postdoctoral tenure at the UK Dementia Research Institute, University of Edinburgh (2017–2025) with Prof Siddharthan Chandran and Prof Josef Priller, Poulomi investigated the cellular and molecular basis of neuroinflammation, a hallmark of many neurological disorders. Her work in Amyotrophic Lateral Sclerosis (ALS) demonstrated cell-autonomous dysfunction of myeloid cells, including microglia and peripheral macrophages, contributing to a pro-inflammatory milieu and accelerated motor neuron degeneration (Banerjee et al., Stem Cell Research, 2021; Journal of Pathology, 2022; Science Advances, 2023). Additionally, Poulomi explored the effect of proteinopathies, particularly tau accumulation, on microglial inflammation and synaptic dysfunction in the context of Progressive Supranuclear Palsy (PSP), a pure form of tauopathy.

Beyond neurodegeneration, Poulomi studied neuron–microglia interactions in Fragile X Syndrome (commonest known genetic cause of Autism and intellectual disability) using patient-derived iPSC microglia, showing that microglial activation drives neuronal hyperexcitability (Banerjee et al., bioRxiv, 2024). Collectively, her research highlights neuroinflammation as a contributory mechanism across neurodegenerative and neurodevelopmental disorders.

Research Focus

The burden of non-communicable neurological disorders in India has nearly doubled over the past three decades, thereby highlighting a pressing need to identify novel disease-modifying strategies. Unravelling how the human brain functions and why it breaks down in disease remains one of the most dynamic areas of neuroscience research.

While neurodegenerative diseases like Alzheimer’s and Parkinson’s are known to affect neurons, recent research shows that the supporting cells in brain—called glial cells—also play a major role. When these cells don’t function properly, they can trigger inflammation, reduce support to neurons, and contribute to neuronal damage. To this end, neuroinflammation characterised by dysfunction of myeloid-lineage cells—such as CNS-resident microglia and circulating monocytes and macrophages, has become one of the key pathologies in neurological diseases. Importantly, the myeloid cell signature—particularly from blood—may serve as a biological indicator of disease stage, offering a path toward scalable, non-invasive diagnostic tests for detecting and characterizing neurological disorders. Separately, genetics plays an important factor in determining the vulnerability of an individual to neurological diseases —but most studies so far have focused on European populations, leaving a gap in understanding how they affect diverse population, including those in India.

Poulomi’s lab at SKAN RT is currently focusing on Parkinson’s disease (PD), a common neurodegenerative disorder that affects a significant number of individuals in India and currently lacks effective disease-modifying therapies. PD is characterized by α-synuclein accumulation and loss of dopaminergic neurons, leading to motor and non-motor symptoms, with growing evidence linking neuroinflammation to disease progression. While PD predominantly affects older adults, early-onset PD (EOPD), diagnosed before 40–50 years of age, accounts for 10–20% of cases and has a strong genetic basis. Notably, studies from India report a higher incidence of EOPD; however, the underlying genetic drivers and the role of neuroinflammation in Indian PD remain poorly understood.

Current Research Objectives

  1. Map the molecular signatures of brain ageing in the Indian population using post-mortem brain tissue from individuals without neurological disease
  2. Map genotype–phenotype relationships in early-onset Parkinson’s disease using genetics and blood-based markers
  3. Identify molecular mechanisms in early neuron–microglia interactions in early-onset Parkinson’s disease using patient iPSC-derived brain cells.

Publications

  1. Banerjee, P., Das Sharma, S., Burr, K., Morris, K., Ritakari, T., Baxter, P., Cooper, J., Cardinalli, A., Subash, S., Paza, E., Story, D., Chattarji, S., Kind, P. C., Carragher, N. O., Thangaraj Selvaraj, B., Priller, J., & Chandran, S. (2024). Human induced pluripotent stem cell-derived microglia contribute to the pathophysiology of Fragile X syndrome via increased RAC1 signaling. 10.1101 (Under review)
  2. Banerjee, P., Mehta, A.R., Nirujogi, R.S., et al. 2022. Cell-autonomous immune dysfunction driven by disrupted autophagy in C9orf72-ALS iPSC-derived microglia contributes to neurodegeneration. Sci. Adv.9, eabq0651(2023). DOI: 10.1126
  3. Kenkhuis, B., van Eekeren, M., Parfitt, D. A., Ariyurek, Y., Banerjee, P., Priller, J., van der Weerd, L., & van Roon-Mom, W. (2022). Iron accumulation induces oxidative stress, while depressing inflammatory polarization in human iPSC-derived microglia. Stem cell reports, 17(6), 1351–1365.
  4. Banerjee, P, Elliott, E, Rifai, O, O’shaughnessy, J, Mcdade, K, Abrahams, S, Chandran, S, Smith, C & Gregory, JM 2021, ‘NLRP3 inflammasome as a key molecular target underlying cognitive resilience in amyotrophic lateral sclerosis’, The Journal of Pathology 256(3), 262–268.
  5. Perkins, E. M., Burr, K., Banerjee, P., Mehta, A. R., Dando, O., Selvaraj, B., Suminaite, D., Nanda, J., Henstridge, C. M., Gillingwater, T. H., Hardingham, G. E., Wyllie, D. J. A., Chandran, S., & Livesey, M. R. (2021). Altered network properties in C9ORF72 repeat expansion cortical neurons are due to synaptic dysfunction. Molecular Neurodegeneration, 16(1),13.
  6. Banerjee, P., Paza, E., Perkins, E. M., James, O. G., Kenkhuis, B., Lloyd, A. F., Burr, K., Story, D., Yusuf, D., He, X., Backofen, R., Dando, O., Chandran, S., & Priller, J. (2020). Generation of pure monocultures of human microglia-like cells from induced pluripotent stem cells. Stem Cell Research, 49, 102046.
  7. Banerjee, P., Surendran, H., Bharti, K., Morishita, K., Varshney, A., & Pal, R. (2018). Long Noncoding RNA RP11-380D23.2 Drives Distal-Proximal Patterning of the Lung by Regulating PITX2 Expression. STEM CELLS, (Dayton, Ohio), 36(2), 218–229.
  8. May-Simera, H. L., Wan, Q., Jha, B. S., Hartford, J., Khristov, V., Dejene, R., Chang, J., Patnaik, S., Lu, Q., Banerjee, P., Silver, J., Insinna-Kettenhofen, C., Patel, D., Lotfi, M., Malicdan, M., Hotaling, N., Maminishkis, A., Sridharan, R., Brooks, B., … Bharti, K. (2018). Primary Cilium-Mediated Retinal Pigment Epithelium Maturation Is Disrupted in Ciliopathy Patient Cells. Cell Reports, 22(1), 189–205.
  9. Shetty, R., Joshi, D., Jain, M., Vasudevan, M., Paul, J. C., Bhat, G., Banerjee, P., Abe, T., Kiyonari, H., Vijayraghavan, K., & Inamdar, M. S. (2018). Rudhira/BCAS3 is essential for mouse development and cardiovascular patterning. Scientific Reports, 8(1), 5632.
  10. Banerjee, P., Dutta, S., & Pal, R. (2016). Dysregulation of Wnt-Signaling and a Candidate Set of miRNAs Underlie the Effect of Metformin on Neural Crest Cell Development. STEM CELLS, (Dayton, Ohio), 34(2), 334–345.
  11. Banerjee, P., Surendran, H., Chowdhury, D. R., Prabhakar, K., & Pal, R. (2016). Metformin mediated reversal of epithelial to mesenchymal transition is triggered by epigenetic changes in E-cadherin promoter. Journal of Molecular Medicine. 94(12), 1397–1409.
  12. Banerjee, P., Venkatachalam, S., Mamidi, M. K., Bhonde, R., Shankar, K., & Pal, R. (2015). Vitiligo patient-derived keratinocytes exhibit characteristics of normal wound healing via epithelial to mesenchymal transition. Experimental Dermatology, 24(5), 391–393
  13. Banerjee, P., Bhonde, R. R., & Pal, R. (2013). Diverse roles of metformin during peri-implantation development: Revisiting novel molecular mechanisms underlying clinical implications. Stem Cells and Development. 22(22), 2927–2934.

Additional Information

Invited Talk:

  • Invited Flash talk at Stem Cell Models of Neurodegeneration (SCMND), Edinburgh, 2025
  • Invited speaker for Women in Autophagy (WIM) network; 2025
  • Invited speaker for Gulmohar postdoc series (arranged by National Centre of Biological Sciences, India) 2025
  • Invited speaker for ENCALS (European Network to Cure ALS) 2022: Cell-autonomous immune dysfunction driven by disrupted autophagy in C9orf72 -ALS iPSC-derived microglia contribute to neurodegeneration.
  • Flash talk in EMBO microglia workshop 2021 and UKDRI Connectome 2021: Disrupted autophagy leads to cell autonomous immune dysfunction in human iPSC-derived C9orf72-ALS microglia.

Grants

🏆  Rising Star Award from International Brain Research Organisation (IBRO), 2025

🏆  RS MacDonald Seed Corn Award, Edinburgh Neuroscience, 2021

Press Releases

  • Boosting brain immune cell waste clearance could provide new drug target for MND, UK Dementia Research Institute (UKDRI), 21 April 2023 Link for details
  • India’s 2025 IBRO Rising Stars: In conversation with Poulomi Banerjee and Proloy Das, Indian Bioscience, 15 September 2025 Link for details

Professional Profiles

Google Scholar link: google scholar
ORCID : 0000-0002-0987-6442

Collaborations

  • Dr Jyoti Nangalia, Group Leader, Wellcome Sanger Institute, United Kingdom
  • Dr Vikram Holla, Department of Neurology, National Institute of Mental Health and Neuro Sciences (NIMHANS)
  • Dr. Pramod Kumar Pal, Senior Consultant-Parkinson’s Disease and Movement Disorders, Happiest Health Systems Pvt. Ltd. and SKAN-RT