The research, the first longitudinal study to use such advanced genomics, now provides investigators with a new target for therapeutic intervention in Parkinson’s disease.

The researchers claim their finding suggests the blood brain barrier, which generally acts as a filter to protect the brain against toxins that have found their way into the systemic circulation but allows the passage of nourishing nutrients into the brain, doesn’t work optimally in some patients with Parkinson’s disease.

The study shows, in a subset of patients with moderately severe Parkinson’s Disease this critical vascular barrier prevents toxins from leaving the brain and inhibits essential nutrients such as glucose from entering it.

The finding could help explain an earlier outcome of the same study, in which the drug nilotinib was able to halt motor and non-motor (cognition and quality of life) decline in the long term.

Nilotinib inactivated a protein (DDR1) that was destroying the ability of the blood brain barrier to function properly. When DDR1 was inhibited, normal transport of molecules in and out of the brain filter resumed, and inflammation declined to the point that dopamine, the neurotransmitter depleted by the disease process, was being produced again.

“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.”

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