Pretty wild.
Researchers of the German Center for Neurodegenerative Diseases (DZNE) have found that “alpha-synuclein,” a protein involved in a series of neurological disorders including Parkinson’s disease, is capable of travelling from brain to stomach and that it does so following a specific pathway. Donato Di Monte and co-workers report on this in the journal Acta Neuropathologica. Their study, carried out in rats, sheds new light on pathological processes that could underlie disease progression in humans.
Alpha-synuclein occurs naturally in the nervous system, where it plays an important role in synaptic function. However, in Parkinson’s disease, dementia with Lewy bodies and other neurodegenerative diseases termed “synucleinopathies,” this protein is accumulated within neurons, forming pathological aggregates. Distinct areas of the brain become progressively affected by this condition. The specific mechanisms and pathways involved in this widespread distribution of alpha-synuclein pathology remain to be fully elucidated. Clinical and experimental evidence suggests however that alpha-synuclein — or abnormal forms of it — could “jump” from one neuron to another and thus spread between anatomically interconnected regions.
Alpha-synuclein lesions have also been observed within neurons of the peripheral nervous system, such as those in the gastric wall. In some Parkinson’s patients, these lesions were detected at early disease stages. “Based on these intriguing observations, it has been hypothesized that the pathological process underlying Parkinson’s disease may actually start in the gastrointestinal tract and then move toward the brain,” Professor Di Monte says. “Our present approach was to look at this long-distance transmission of alpha-synuclein from the opposite perspective, investigating the possibility that alpha-synuclein may travel from the brain to the gut.”
