Skip to main content
Blizard Institute - Faculty of Medicine and Dentistry

Dr Agnes Nishimura, PhD


Non-Clinical Lecturer in Neuroscience

Telephone: 020 7882 2685
Twitter: @NishimuraAgnes


Dr Agnes Nishimura graduated in Biological Sciences at University of Sao Paulo, Brazil, and she completed her PhD in human genetics in the same institution. During her PhD, she identified a rare mutation leading to an atypical form of motor neurone disease (MND) in the Brazilian population. She moved to London to work with Prof. Christopher Shaw at King’s College London to continue her career on MND research. There, she continued to work with genetics of MND, but also explored modelling MND using induced pluripotent stem cells (iPSCs). In the past five years, Agnes has been working on a biobank of iPSCs from patients with MND in collaboration with the Motor Neurone Disease Association. She has contributed to teaching and supervision at postgraduate level at KCL and she became a fellow of the Higher Education Academy (FHEA). Furthermore, she has editorial experience as a re-viewer, and became associate editor of Frontiers of Cellular Neuroscience in 2021.




1. Co-convenor of BSc Neuroscience Year 2 (BMD265 Systems Neuroscience)

2. Co-convenor for Research Projects

3. Academic advisor

4. PBL tutor


Research Interests:

Dr Nishimura research focus on neurodegeneration, in particular motor neurone disease (MND). She is interested in identifying disease mechanisms using induced pluripotent stem cells, as well as other cellular models.

Specific areas of interest:

· Understanding human diseases (From genes to proteins)

· Genetics of neurodegenerative diseases

· stem cells research

  - Disease modelling using induced pluripotent stem cells

  - 2D and organoids

· mRNA dysregulation

· vesicular transport

· protein misfolding and clearance

· stress and inflammation

· synaptopathy

· Drug screening


  1. Generation of six induced pluripotent stem cell lines from patients with amyotrophic lateral sclerosis with associated genetic mutations in either FUS or ANXA11. Hedges EC, Topp S, Shaw CE, Nishimura AL. Stem Cell Res. 2021 Apr;52:102246. doi: 10.1016/j.scr.2021.102246. Epub 2021 Feb 12.
  2. Mutant induced pluripotent stem cell lines recapitulate aspects of TDP-43 proteinopathies and reveal cell-specific vulnerability. Bilican B, Serio A, Barmada SJ, Nishimura AL, Sullivan GJ, Carrasco M, Phatnani HP, Puddifoot CA, Story D, Fletcher J, Park IH, Friedman BA, Daley GQ, Wyllie DJ, Hardingham GE, Wilmut I, Finkbeiner S, Maniatis T, Shaw CE, Chandran S. Proc Natl Acad Sci U S A. 2012 Apr 10;109(15):5803-8. doi: 10.1073/pnas.1202922109. Epub 2012 Mar 26
  3. Nuclear import impairment causes cytoplasmic trans-activation response DNA-binding protein accumulation and is associated with frontotemporal lobar degeneration. Nishimura AL, Zu-punski V, Troakes C, Kathe C, Fratta P, Howell M, Gallo JM, Hortobágyi T, Shaw CE, Rogelj B. Brain. 2010 Jun;133(Pt 6):1763-71. doi: 10.1093/brain/awq111. Epub 2010 May 14.
  4. Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6. Vance C, Rogelj B, Hortobágyi T, De Vos KJ, Nishimura AL, Sreedharan J, Hu X, Smith B, Ruddy D, Wright P, Ganesalingam J, Williams KL, Tripathi V, Al-Saraj S, Al-Chalabi A, Leigh PN, Blair IP, Nicholson G, de Belleroche J, Gallo JM, Miller CC, Shaw CE. Science. 2009 Feb 27;323(5918):1208-1211. doi: 10.1126/science.1165942. 5
  5. A mutation in the vesicle-trafficking protein VAPB causes late-onset spinal muscular atrophy and amyotrophic lateral sclerosis. Nishimura AL, Mitne-Neto M, Silva HC, Richieri-Costa A, Middleton S, Cascio D, Kok F, Oliveira JR, Gillingwater T, Webb J, Skehel P, Zatz M. Am J Hum Genet. 2004 Nov;75(5):822-31. doi: 10.1086/425287. Epub 2004 Sep 15.


Back to top