UF Department of Neuroscience assistant professor, Paramita Chakrabarty, Ph. D., and her research team has reported their new findings in npj Parkinson’s Disease that an anti-inflammatory cytokine, Interleukin 10, has a profound detrimental effect in a mouse model of Parkinson’s disease. This study was co-authored by Samuel Cockey, an undergraduate trainee, supported by the University Scholar Program and is now currently in a post-baccalaureate program at NIH.
The research showed that, contrary to expectations, this anti-inflammatory cytokine worsened intracellular protein deposits in the nervous system and reduced survival in mice that were injected with disease-inducing aggregates of the α-synuclein protein. “This helps us to take a major step in elucidating the complex relationship between immune signaling and neurodegenerative diseases,” says Chakrabarty.
Overall, their research demonstrates ‘unexpected adverse effects of Il-10, especially its immunosuppressive variant, I87A Il-10, in a mouse model of PD, highlighting the pleiotropic functions of immune mediators and their complex role in non-cell autonomous signaling in neurodegenerative proteinopathies.’
This research is part of the emerging observations in neurodegenerative dementias that neuroimmune signaling can have unexpected outcomes. “Simply suppressing inflammatory activation may not be enough to stop the progression of disease in these diseases,” says Chakrabarty.
Chakrabarty lab focuses on neuro-immune interactions in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and ALS through highly collaborative research conducted at CTRND, MBI and department of Neuroscience.