Parkinson’s disease is a brain disorder characterized by problems with movement and by a loss of neuronal cells in the substantia nigra of the midbrain that produce the neurotransmitter dopamine. Its causes are not clear, although some evidence suggests that disrupted immune function and inflammation, possibly in the gut, might have a part to play. Two proteins, PINK1 and parkin, regulate the function of energy-generating organelles in the cell called mitochondria
1–
3, and are dysfunctional in certain forms of Parkinson’s disease.
Writing in Nature,Matheoud
et al.4 show that, in mice lacking PINK1, an intestinal infection can trigger an immune response that results in the production of immune cells that target mitochondrial molecules. This response also causes transient motor impairments resembling those in Parkinson’s disease and a temporary loss of neuronal dopamine-release sites.
Mutations in the genes encoding PINK1 and parkin have been linked to rare, heritable members of parkinsonian syndromes
5–
7, the group of disorders to which Parkinson’s disease belongs. However, these proteins were long considered mostly irrelevant for the approximately 90% of cases of Parkinson’s disease that occur later in life (known as idiopathic Parkinson’s disease), and which are thought to arise from complex interactions between genes and the environment
8.
