Quite a few neurological disorders remain mysteries even when we know so much about them. Parkinson’s diseases (PD) is one of them. Dopamine deficiency is the established final common pathway, but why this deficiency presents in different ways is unclear. PD variants such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and Lewy body disease (LDB) have distinct clinical features to confound any common cause. What then causes dopamine deficiency in the first place?
One link researchers are looking at is the possibility of a pathogen travelling up to the brain from the gut via the vagus nerve. This report from the Annals of Neurology suggests this hypothesis; the researchers found a reduced risk of PD in patients who have had the main trunk of the vagus nerve severed (vagotomy). For more details see a full analysis of the study here.
Clearly we can’t recommend vagotomy to our at-risk PD patients, and neither can we recommend gout! Yes, studies have suggested that PD patients have a low uric acid level, and this predates the disease onset. Another study takes things further to suggest that uric acid is neuroprotective because of its antioxidant effect. This long list of PubMed abstracts shows the proliferating research into uric acid.
And finally, again from the Annals of Neurology, is a paper reporting increased creativity in people with PD on dopamine replacement treatment. The study compares people with PD on treatment to control subjects. It is however not clear if the creativity is a feature of PD, or of its treatment.
Just a few curious things