Sonia George, Ph.D.

Patrik Brundin Laboratory
Sonia George, Ph.D.
Research scientist


Dr. Sonia George received her Ph.D. in neuroscience from the University of Melbourne, where she studied animal models of Parkinson’s disease, further characterizing and using the transgenic A53T alpha-synuclein mouse to model Parkinson’s disease. Sonia started her work focusing on previously undescribed behavioral abnormalities in these animals. In 2009, she began working with other transgenic models of Parkinson’s disease to further understand disease mechanisms while a postdoctoral researcher at Johns Hopkins University and University of Minnesota. Sonia then moved to Lund University to focus her research on Alzheimer’s disease, the leading cause of late-onset dementia. Using a transgenic mouse model of Alzheimer’s disease, she tested potential therapeutics and also studied the stereotypical spread of pathology over time in a mouse model of Alzheimer’s disease. Using a neurotoxin to chemically kill the brain cells in the brain structure where pathology first appears this model, Sonia prevented the further spread of pathology. In the Brundin Laboratory at Van Andel Research Institute, she continues using her skills to model Parkinson’s disease in mice to elucidate disease mechanisms, test potential therapeutics and investigate the role of inflammation in the spread of brain pathology in this disease.


Research Focus

Dr. George investigates the mechanisms of neurodegeneration in Parkinson’s disease. Currently, she is studying the role of neuroinflammation and its contribution to Parkinson’s disease.


Ph.D. in neuroscience, University of Melbourne (with Janetta G. Culvenor, Ph.D.)
Postdoc: with Patrik Brundin, M.D., Ph.D., and Roger Olsson, Ph.D., Lund University
Postdoc: with Michael Lee, Ph.D., University of Minnesota

Selected publications

Bacelis J, Compagno M, George S, Pospisilik JA, Brundin P, Naluai ÅT, Brundin L. 2021 Decreased risk of Parkinson’s disease after rheumatoid arthritis diagnosis: A nested case-control study with matched cases and controls. J Parkinsons Dis 11:82

George S, Tyson T, Rey NL, Sheridan R, Peelaerts W, Becker K, Schulz E, Meyerdirk L, Burmeister AR, von Linstow CU, Steiner JA, Galvis MLE, Ma J, Pospisilik JA, Labrie V, Brundin L, Brundin P. 2021 T cells limit accumulation of aggregate pathology following intrastriatal injection of α-synuclein fibrils. J Parkinsons Dis 11:585

George S, Rey NL, Tyson T, Esquibel C, Meyerdirk L, Schulz E, Pierce S, Burmeister AR, Madaj Z, Steiner JA, Escobar Galvis ML, Brundin L, Brundin P. 2019. Microglia affect α-synuclein cell-to-cell transfer in a mouse model of Parkinson’s disease. Mol Neurodegener. 14:34. 

Tyson T, Senchuk M, Cooper JF, George S, Van Raamsdonk JM, Brundin, P. 2017. Novel animal model defines genetic contributions for neuron-to-neuron transfer of α-synuclein. Sci Rep 7:7506.

Ghosh A, Tyson T, George S, Hildebrandt EN, Steiner JA, Madaj Z, Escobar Galvis ML, Van Raamsdonk JM, McDonald WG, Colca JR, Brundin P. 2016. Mitochondrial pyruvate carrier regulates autophagy, neurodegeneration and inflammation in models of Parkinson’s disease. Science Transl Med 8: 368ra174.

George S, Ronnback A, Gouras GK, Petit GH, Grueninger F, Winblad B, Graff C, Brundin P. 2014. Inhibiting the spread of amyloid beta pathology in a mouse model of Alzheimer’s disease. Acta Neuropathol Comm 2:17.

George S, Gouras GK, Petit GH, Brundin P, Olsson R. 2013. Nonsteroidal selective androgen and estrogen receptor modulating compounds moderate cognitive deficits and amyloid-β levels in a mouse model of Alzheimer’s disease. ACS Chem Neurosci 4(12):1537–1548.

George S, Mok SS, Nurjono M, Ayton S, Finkelstein DI, Masters CL, Li Q-X, Culvenor JG. 2010. α-synuclein transgenic mice reveal compensatory increases in Parkinson’s disease associated proteins DJ-1 and Parkin and have enhanced α-synuclein and PINK1 levels after rotenone treatment. J Mol Neurosci42(2):243–254.

George S, van den Buuse M, Mok SS, Masters CL, Li Q-X, Culvenor JG. 2008. α-synuclein transgenic mice exhibit reduced anxiety-like behaviour. Exp Neurol 210(2):788–792.