http://www.eurekalert.org/pub_releases/ ... 082911.php
Jefferies, in an article published online today by PLoS One, theorizes that the profusion of blood vessels is stimulated by amyloid beta, a protein fragment that has become a hallmark of Alzheimer's disease. The blood vessel growth, or "neo-angiogenesis," leads to a breakdown of the blood-brain barrier – the tightly interlocked network of cells that allows oxygen-carrying blood to reach brain tissue while blocking harmful substances, such as viruses.
"When the blood vessels grow, the cells of the vessel walls propagate by dividing," Jefferies says. "In the process of splitting into two new cells, they become temporarily rounded in shape, and that undermines the integrity of the blood-brain barrier, potentially allowing harmful elements from outside the brain to seep in."
The deterioration of the barrier might in turn allow the depositing of amyloid beta, which accumulates around neurons and eventually kills them.
Here we go: Alzheimer's has something to do with BBB and blood vessels... in this case they think there are too MANY blood vessels.
It seems like vascular components are important.
But I looked for publications of dr. Jefferies and found this one: http://www.ncbi.nlm.nih.gov/pubmed/20832870
Multiple sclerosis (MS) is a demyelinating disease characterized by the breakdown of the blood-brain barrier (BBB), and accumulation of inflammatory infiltrates in the central nervous system. Tight junctions are specialized cell-cell adhesion structures and critical components of the BBB that have previously been shown to be abnormally distributed in MS tissue. To evaluate whether experimental autoimmune encephalomyelitis (EAE) provides a suitable model for this aspect of MS disease, we examined the expression and distribution of ZO-1 over the course of disease in EAE. We observed a dramatic relocalization of ZO-1 which precedes overt clinical disease and correlates with the sites of inflammatory cell accumulation.Treatment of in vitro cultures of murine brain endothelial cells with components of EAE induction provided similar findings, with relocalization of ZO-1 and increased permeability of endothelial monolayers. BBB disruption in the EAE model appears to parallel disease progression in MS, with direct effects on the cerebrovascular endothelium, making it an ideal tool for future evaluation of tight junction breakdown and repair in MS-like pathology.
It looks like we don't need CCSVI to damage the endothelium... this one looks like a bad news for us is'nt it?