A defect in the blood-brain barrier may play a role in Parkinson’s disease, according to groundbreaking research discovery.
Researchers at Georgetown University Medical Center say their finding, detailed in a study published earlier this month in Neurology Genetics, suggests that blood vessel walls called the blood-brain barrier doesn’t work correctly in some Parkinson’s patients.
When it’s working properly, the blood-brain barrier acts as a filter, keeping toxins out while allowing nutrients to reach the brain. When the barrier fails, however, toxins are trapped in the brain, preventing glucose and other nutrients from entering. A dysfunctional barrier also allows inflammatory cells and molecules from the body to enter the brain and cause damage.
“Much work remains to be done, but just knowing that a patient’s brain vascular system is playing a significant role in the progression of the disease is a very promising discovery,” senior study author Charbel Moussa said in a university news release.
According to the news release, the research could lead to new treatments for Parkinson’s disease and could help explain previous findings that the drug nilotinib, a leukemia drug, was linked to a reduction in movement problems and an increase in quality of life in Parkinson’s patients.
“To our knowledge, this is the first study to show that the body’s blood-brain barrier potentially offers a target for the treatment for Parkinson’s disease,” Moussa said.
The new discovery comes from a clinical trial that featured comprehensive genome analysis of 75 patients with severe Parkinson’s disease. The results were compared before and after receiving off-label treatment with nilotinib or a placebo.
“Not only does nilotinib flip on the brain’s garbage disposal system to eliminate bad toxic proteins, but it appears to also repair the blood-brain barrier to allow this toxic waste to leave the brain and to allow nutrients in,” Moussa said.
“Parkinson’s disease is generally believed to involve mitochondrial or energy deficits that can be caused by environmental toxins or by toxic protein accumulation. It has never been identified as a vascular disease,” he added.
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