Baijayanta Maiti, MD, PhD

Assistant Professor of Neurology

Phone: 314-362-6908
Fax: 314-747-3258


  • Medical Degree: Calcutta Medical College, Calcutta, India
  • PhD: Human Genetics: University of Utah, Salt Lake City, UT
  • Residency: Washington University School of Medicine, St. Louis, MO
  • Fellowship: Neuromuscular Medicine: Washington University School of Medicine, St. Louis, MO
  • Fellowship: Movement Disorders: Washington University School of Medicine, St. Louis, MO

Board Certifications

  • Neurology
  • Neuromuscular Medicine


  • 2017: American Academy of Neurology and American Brain Foundation Clinical Research Training Fellowship in Parkinson’s Disease, funded by AbbVie.
  • 2016: Parkinson Study Group (PSG) Mentoring Committee membership.
  • 2016: Parkinson Study Group/Parkinson’s Disease Foundation Mentored Clinical Research Award, supported by Parkinson Study Group (PSG) and Parkinson’s Disease Foundation’s (PDF) Advancing Parkinson’s Treatments Innovations Grant.
  • 2012: Neurology Student Clerkship Teaching Honor Roll, Washington University in St. Louis School of Medicine
  • 2008: Award for poster presentation at the New Directions in Biology and Disease of Skeletal Muscle meeting in New Orleans, Louisiana.
  • 2007: Elsevier WMS award for poster presentation at the 12th International Congress of the World Muscle Society, Sicily, Italy.
  • 2007: Fellowship for Young Scientist travel award, administered by the World Muscle Society, 12th International Congress of the World Muscle Society, Sicily, Italy.
  • 2007, 2006 and 2005: Graduate Research Travel Awards (3), awarded by University of Utah.
  • 1996 and 1994: National Scholarships (2), Government of West Bengal, India.

Clinical Interests

Dr. Maiti is a fellowship trained Movement Disorders specialist. His clinical practice focuses on patients with Parkinson disease, dystonia, other movement disorders as well as the administration of botulinum toxin for dystonia, sialorrhea and cerebral palsy.

Research Interests

Dr. Maiti’s research utilizes state of the art multimodal, non-invasive, functional imaging techniques to enhance our understanding of the pathophysiologic bases of dementia and gait impairment in Parkinson disease and thereby unravel new therapeutic targets.


  1. Lucero, C., Campbell M.C., Flores, H., Maiti, B., Perlmutter, J.S., Foster, E.R. (2015). Cognitive reserve and b-amyloid pathology in Parkinson disease. Parkinsonism Relat Disord. 21(8): 899-904.
  2. Wein N., Vulin, A., Falzarano, MS., Al-Khalili, Szigyarto C., Maiti, B., Findlay, A.R., Uhlen, M., Bakthavachalu, B, Messina, S., Vita, G., Gualandi, F., Wilton, SD., Dunn, DM., Shoenberg, D., Weiss, R.B., Howard, M.T., Ferlini, A. Flanigan, K.M. (2014).Translation from a DMD exon 5 IRES results in a functional dystrophin isoform that attenuates dystrophinopathy in humans and mice. Nat Med 20(9), 992-1000.
  3. Maiti, B., Bucelli, RC. (2014). Atypical CSF findings in West Nile neuroinvasive disease, a diagnostic and therapeutic conundrum. Neurol Neuroimmunol Neuroinflammation 1(1), e8. doi: 10.1212/NXI.0000008
  4. Vulin, A., Wein N., Strandjord, D.M., Findlay, A.R., Johnson, E.K., Maiti, B., Howard, M.T., Kaminoh, Y.J., Taylor, L.E., Simmons, T.R., Ray, W.C., Montanaro, F., Ervasti, J.M. and Flanigan, K.M. (2014). The ZZ domain of dystrophin: making sense of missense mutations. Hum Mutat 35(2), 257-264.
  5. Maiti, B., Arbogast, S., Allamand, V., Moyle, M.W., Anderson, C.B., Richard, P., Guicheney, P., Ferreiro, A., Flanigan, K.M., Howard, M.T. (2009). A mutation in the SEPN1 selenocysteine redefinition element (SRE) reduces selenocysteine incorporation and leads to SEPN1-related myopathy. Hum Mutat 30, 411-416.
  6. Gurvich, O.L., Maiti, B., Weiss, R.B., Aggarwal, G., Howard, M.T., Flanigan, K.M. (2009).
  7. DMD exon 1 truncating point mutations: amelioration of phenotype by alternative translation initiation in exon 6. Hum Mutat 30, 633-640. (PMID: 19206170)
  8. Schessl, J., Taratuto, A.L., Sewry, C., Battini, R., Chin, S.S., Maiti, B., Dubrovsky, A.L., Erro, M.G., Espada, G., Robertella, M., Saccoliti, M., Olmos, P., Bridges, LR., Standring P., Hu, Y., Zou, Y., Swoboda, KJ., Scavina, M., Goebel, HH, Mitchell, CA., Flanigan, KM., Muntoni, F., Bonemann, CG. (2009). Clinical, histological and genetic characterization of reducing body myopathy caused by mutations in FHL1. Brain 132, 452-464.
  9. Schessl, J., Zou, Y., McGrath, M.J., Cowling, B.S., Maiti, B., Chin, S.S., Sewry, C., Battini, R., Hu, Y., Cottle, D.L., Rosenblatt, M., Spruce, L., Ganguly, A., Kirschner, J., Judkins, AR., Golden, JA., Goebel, HH., Muntoni, F., Flanigan, KM., Mitchell, CA., Bonnemann, CG. (2008). Proteomic identification of FHL1 as the protein mutated in human reducing body myopathy. J Clin Invest 118, 904-912.