A recent study has found that individuals with chronic hepatitis B and C infections may have more to worry about; they may also be at increased risk for developing Parkinson’s disease. Not only this, but another study found that changes in the microbiome may also elicit the development of the disease.
The Centers for Disease Control and Prevention estimate that chronic hepatitis B plagues about 850,000 to 2.2 million individuals in the United States alone, and a staggering 2.7 to 3.9 million individuals are infected with chronic hepatitis C. Many individuals experience only a few symptoms and therefore may not seek out healthcare professionals, which can prevent diagnosis and needed treatment.
The results of a recent study published in the journal Neurology show that there may be a link between chronic hepatitis infection and the development of Parkinson’s disease. For the study, the researchers reveiwed the medical records of patients with “a first case of hepatitis B (~22,000 patients), hepatitis C (~48,000 patients), autoimmune hepatitis (~6,000 patients), chronic active hepatitis (~4,000 patients), and HIV (~20,000 patients) between 1999 and 2011” from a British database. They compared these patients with others who had “relatively minor conditions,” such as bunions, cataract surgery, or knee replacement surgery (~6,000 patients), and noted which patients later developed Parkinson’s disease.
The results of their comparison? Those patients with hepatitis B infection were 76% more likely to develop Parkinson’s disease than those falling in the “relatively minor conditions” category, while those with hepatitis C infection were 51% more likely to develop the disease. Patients with autoimmune hepatitis, chronic active hepatitis, and HIV did not show an “increased rate of Parkinson’s disease.”
Another recent study, published in the journal, Cell, provides another look at how Parkinson's potentially develops. The researchers on this study theororize that the disease does not start in the brain at all. Rather, it begins in the gut and later travels to the brain, resulting in the tremors and motion problems that are commonly associated with the disease.
By taking a closer look at the “spread of toxic fibres” made of alpha-synuclein molecules, which tend to “clump together and form fibres that damage the nerves in the brain,” the findings suggest that neurodegenerative disease might originate in the gut, not just in the brain.
For this study, the researchers genetically modified mice “by over-producing alpha-synuclein fibers,” thus, increasing their susceptibility to Parkinson’s disease, and placed them in three different environments: normal, non-sterile cages, or sterile germ-free cages.
Their findings? The mice held in the sterile cages expressed less “motor deficits” and a smaller number of toxic fibers in their brains, while the mice held in the non-sterile cages went on to develop Parkinson’s disease, just as they had been modified to do. Treatment with antibiotics managed to reduce disease symptoms in the mice held in non-sterile cages, which, according to the researchers, is suggestive of “something in their microbiome that was enhancing the symptoms.”
The research team also injected the germ-free mice with gut bacteria from humans who had Parkinson’s disease. According to the press release, these mice “quickly went from showing hardly any symptoms to deteriorating rapidly.”
The researchers feel that the gut microbiota might “regulate” the associated symptoms of the disease; the bacteria may also prompt the release of chemicals that results in overactivation of the brain, which leads to neurological damage. The findings may provide some way to inform treatment options, but there is still much more research that needs to be done “before we can say for sure what’s going on,” the researchers admitted.