Posted by jrbecker on June 3, 2003, at 23:12:03
In reply to Re: HPA aix and non-suppression » jrbecker, posted by Pfinstegg on June 2, 2003, at 11:37:22
As an addendum to the discussion before about the role of CRF and atypical depression. I found this to be interesting...
http://www.acnp.org/g5/p/SCH7_91-108.pdf
"Non-peptide CRF-binding Protein Ligand Inhibitors
As mentioned above, the CRF-binding protein has the capacity to bind and functionally inactivate CRF. Peptide CRF-BP ligand inhibitors release CRF from the binding protein, making it available for binding to its receptor. These inhibitors have been theorized to have efficacy in diseases that are associated with low levels of CRF, such as Alzheimer's disease (6). Interestingly, in contrast to the direct i.c.v. administration of CRF, inhibition of the CRF-BP by ligand inhibitors that release functional CRF does not cause anxiogenic-like activity in animal models, validating the approach for diseases that require an increase in CRF function (6). Thus, compounds that dissociate CRF from its binding protein complex will selectively increase synaptic concentrations of CRF in discrete brain regions and may provide a novel treatment opportunity for disorders associated with low levels of CRF. To date however, no non-peptide CRF-BP ligand inhibitors have been discovered to test this hypothesis."
So it seems that there has been some sort of proposed mechanism of action for treating underactive corticotropin-releasing factor output. Unfortunately, we'll have to wait for the engineering of such a compound before it can be determined what role it will have in benefiting conditions such as atypical depression, alzheimer's, etc.
poster:jrbecker
thread:228381
URL: http://www.dr-bob.org/babble/20030530/msgs/231255.html