Thanks Cara for your information.
A Dutch Professor Nico Leenders is doing some exciting work on this topic, see below. He is going to puiblish a new paper soon and has promised to send me a copy. I can't wait to see a copy.
Also, I have received a copy from the author, of the paper by Brinda S. Desai, called BBB Pathology in AD and PD, Cell Transplantation, Vol 16,pp 285-299, 2007.
Here they review the literature on the BBB, and say both AD and PD share dysfunction of the BBB, and implications of this dysfunction are not widely appreciated.
They show that the BBB in PD can become so permeable, that carbidopa can enter the brain, a possibility I mentioned previously. This of course can prevent conversion of L-dopa to dopamine in the brain.
They point out how there is no adequate explanation of the progressive nature of PD, but the BBB theory gives an explanation. "If the BBB is disrupted, then elements of the peripheral immune systemmight serve as another factor in disease progression."
Ron

Blood-brain barrier dysfunction in Parkinson’s disease
KL Leenders, R Kortekaas, AL Bartels, J Oostrom, A Willemsen, J Bart
S77, P257

The blood-brain barrier is defective in PD patients, according to this study. PET imaging of verapamil was used to measure activity of the P-glycoprotein system, which transports unwanted substances out of the endothelium back into the blood. Comparing five PD patients to five controls, the authors found significant differences in the brain penetration of verapamil (18% higher for PD patients, p=0.02) only in the midbrain region. All patient values were higher than all controls. The authors suggest, “A faulty BBB function on the basis of genetic predisposition might in the course of years allow toxic compounds—or compounds normally circulating in the blood but not passing the BBB—to enter the brain in certain regions and damage vulnerable cells.”


Abstract
Parkinson's disease (PD) is associated with a loss of neurons from the midbrain. The cause of PD is unknown, but it is established that certain neurotoxins can cause similar syndromes. The brain is normally protected from these noxious blood-borne chemicals by the blood-brain barrier which includes specialized proteins 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 to PD appears codetermined by the genotype for the P-gp gene. We hypothesized that PD patients have reduced P-gp function in the blood-brain barrier. We used positron emission tomography to measure brain uptake of [11C]-verapamil, which is normally extruded from the brain by P-gp. Here, we show significantly elevated uptake of [11C]-verapamil (18%) in the midbrain of PD patients relative to controls. This is the first evidence supporting a dysfunctional blood-brain barrier as a causative mechanism in PD. Ann Neurol 2005;57:176-179
PMID: 18061888 [PubMed - in process]