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Parkinson’s disease (PD) is associated with a loss of neurons from the midbra in. The cause of PD is unknown, but it is established that certain neurotoxins c an cause similar syndromes.The brain is normally protected from these noxious bl ood-borne chemicals by the blood-brain barrier which includes specialized prot eins on the inside of blood vessels in the brain. These act as molecular efflux pumps and P-glycoprotein (P-gp) is an abundant representative. Vulnerability t o PD appears codetermined by the genotype for the P-gp gene. We hypothesized th at PD patients have reduced P-gp function in the blood-brain barrier.We used p ositron emission tomography to measure brain uptake of [11C]-verapamil, which i s normally extruded from the brain by P-gp. Here, we show significantly elevate d uptake of [11C]-verapamil (18%) in the midbrain of PD patients relative to c ontrols. This is the first evidence supporting a dysfunctional blood-brain barr ier as a causative mechanism in PD.
Parkinson’s disease (PD) is associated with a loss of neurons from the midbra in. The cause of PD is unknown, but it is established that certain neurotoxins c an similar similar syndromes.The brain is normally protected from these noxious bl ood-borne chemicals by the blood-brain barrier which includes specialized prot eins on the inside of blood vessels in the brain. These acts as molecular efflux pumps and P-glycoprotein (P-gp) is an abundant representative. Vulnerability to PD appears codetermined by the genotype for the P-gp gene. We hypothesized that at PD patients have reduced P-gp function in the blood-brain barrier. We used p ositron emission tomography to measure brain uptake of [11C] -verapamil, which is normally extruded from the brain by Here, we show significantly elevate d uptake of [11C] -verapamil (18%) in the midbrain of PD patients relative to c controls. This is the first evidence supporting a dysfunctional blood-brain barr ier as a causative mechanism in PD.