....whether it be meditation, exercise, prayer, hypnosis, massage, etc.

1: Front Biosci. 2007 Jan 1;12:1615-28.

Corticotropin-releasing hormone and the blood-brain-barrier.

Theoharides TC, Konstantinidou AD.

Department of Pharmacology and Experimental Therapeutics, Tufts University
School of Medicine and Tufts-New England Medical Center, 136 Harrison Avenue,
Boston, MA 02111, USA. theoharis.theoharides@tufts.edu

Increased blood-brain-barrier (BBB) permeability precedes any clinical or
pathologic signs and is critical in the pathogenesis of multiple sclerosis (MS)
and brain metastases. CD4+ TH1 cells mediate demyelination in MS, but how they
get sensitized and enter the brain to induce brain inflammation remains obscure.
TH2 cytokines associated with allergic disorders have recently been implicated
in MS, while genes upregulated in MS plaques include the mast cell-specific
tryptase, the IgE receptor (Fc-epsilon-RI) and the histamine-1 receptor. Mast
cell specific tryptase is elevated in the CSF of MS patients, induces
microvascular leakage and stimulates protease-activated receptors (PAR), leading
to widespread inflammation. BBB permeability, MS and brain metastases appear to
worsen in response to acute stress that leads to the local release of
corticotropin-releasing hormone (CRH), which activates brain mast cells to
selectively release IL-6, IL-8 and vascular endothelial growth factor (VEGF).
Acute stress increases BBB permeability that is dependent on CRH and mast cells.
Acute stress shortens the time of onset of experimental alleric
encephalomyelitis (EAE) that does not develop in W/W mast cell deficient or CRH
-/- mice. Brain mast cell inhibition and CRHR antagonists offer novel
therapeutic possibilities.

PMID: 17127408 [PubMed - in process]