Dementia

Natural Killer Cells Could Be Harnessed to Fight Neurodegenerative Disease

Posted on 27 March 2020

Natural killer (NK) cells, a type of white blood cell, could protect against changes in the brain that lead to Parkinson’s disease.

Natural killer cells are white blood cells that are important in the immune response to viruses and to tumour development. Natural killer cells are special because they recognise infected cells by responding to cellular stress. This makes them unique among white cells, which usually require signals from a protein complex called MHC to detect whether a cell is infected or not.

Natural Killer Cell | Natural killer cell function, relation… | Flickr

Research published in PNAS suggests that natural killer cells may play a role in restraining inflammation in the brain and clearing the buildup of toxic proteins, both of which contribute to neurodegenerative disorders. The study found that NK cells were able to degrade misfolded alpha synuclein, a protein that is particularly associated with Parkinson’s disease. Furthermore, when researchers depleted NK cells in mouse models of Parkinson’s disease, the animals had more alpha synuclein deposits, and their disease symptoms were worse.

alpha-Synuclein-based Model for Studying Parkinsons Disease ...
Alpha synuclein aggregates to form Lewy bodies that disrupt neuron function

It is possible that with further study, a neuroprotective effect of natural killer cells could be harnessed to slow neurodegeneration. NK functions are impaired with ageing, so finding ways to maintain this cell population in old age may be a therapeutic avenue. However, studies in animal models of dementia tend to translate poorly to humans, so it remains to be seen whether this research will have clinical implications.


References

‘Natural killer’ cells could halt Parkinson’s progression: https://news.uga.edu/natural-killer-cells-halt-parkinsons-progression/

NK cells clear α-synuclein and the depletion of NK cells exacerbates synuclein pathology in a mouse model of α-synucleinopathy: https://doi.org/10.1073/pnas.1909110117

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