A possible autoimmune feature of Parkinson’s disease is reported this week in Nature. The findings may offer new insights into the causes of Parkinson’s disease.
Neurodegenerative diseases are generally considered not to possess autoimmune features, but genetic studies have linked Parkinson’s disease with variants of the major histocompatibility complex (MHC) genes. MHC proteins bind short fragments of processed proteins and present these on the surface of the cell for sampling by cells of the immune system. Most of these fragments are ignored by the immune system, but some elicit a T cell response - in the case of autoimmunity, inappropriately so.
Parkinson’s disease features aggregates of a protein called alpha-synuclein in nerve cells and is also associated with defects in protein processing. Abnormal processing of proteins could in theory result in the generation and presentation of unusual fragments that would be recognized by, and inadvertently activate, T cells. David Sulzer and colleagues compare samples from 67 patients with Parkinson’s disease and 36 healthy control participants, and report that a defined set of peptides derived from alpha-synuclein can indeed be recognized by T cells from Parkinson’s disease patients but not from healthy participants. These findings suggest that an autoimmune response may underlie Parkinson’s disease and may explain the association of Parkinson’s disease with genetic variants of the MHC genes.
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