Key to Blood-Brain Barrier and could drug Imatinib be used for this?
 

Key to Blood-Brain Barrier Opens Way for Treating Alzheimer’s and Stroke
ScienceDaily (Oct. 15, 2010) — While the blood-brain barrier (BBB) protects the brain from harmful chemicals occurring naturally in the blood, it also obstructs the transport of drugs to the brain. In an article in Nature scientists at the Swedish medical university Karolinska Institutet now present a potential solution to the problem. The key to the BBB is a cell-type in the blood vessel walls called pericytes, and the researchers hope that their findings will one day contribute to new therapies for diseases like Alzheimer's and stroke.


"Our new results show that the blood-brain barrier is regulated by pericytes, and can be opened in a way that allows the passage of molecules of different sizes while keeping the brain's basic functions operating properly," says Christer Betsholtz...

"Another interesting find is that the cancer drug Imatinib, which
inhibits certain signal proteins for cell growth, has a similar effect
in the presence of pericytes in that they also close the capillary
wall transport paths," says Professor Christer Betsholtz.
http://www.sciencedaily.com/releases...1014083341.htm

another use for Imatinib and PD?
 

(all this seems interesting though not applicable at present to me. Have noticed the term "NGF dysfunction ": seems nerve growth dysfunction is the newest "dysfunction theory" in PD. recent reports on DJ1[PARk7] and PD)

http://www.sciencedaily.com/releases...1001163342.htm


Parkinson's: Excess of Protein Suggests New Target for Treatment With
Widely Used Anti-Cancer Drug Imatinib


ScienceDaily (Oct. 4, 2010) ‹ Johns Hopkins scientists have discovered
that the over-activation of a single protein may shut down the
brain-protecting effects of a molecule and facilitate the most common
form of Parkinson's disease...

Previous research demonstrated that a protein called parkin protects
brain cells by "tagging" certain toxic elements that are then destroyed
naturally. It was also known that mutations in the gene that holds the
code for parkin cause rare, familial forms of PD. However, parkin's role
remained unclear in sporadic late-onset PD, the prevalence of which is
increasing as the population ages...
...Results of the new study, published Sept. 7 in the Proceedings of the
National Academy of Sciences (PNAS) Online Early Edition, indicate that
an over-activation of a protein called c-Abl- can shut down the activity
of parkin and contribute to a build-up of toxic proteins that kill brain
cells and enables the progression of PD.


C-Abl contributes to the regulation of cell death and is implicated in a
host of diseases. It has already has proven to be a target for certain
types of cancer-killing drugs, such as imatinib (Gleevec), the first
drug designed to directly switch off a biochemical signal that directly
targets a protein vital to cancer growth, says Ted Dawson, M.D., Ph.D...