“Conclusion A number of genetic and environmental insults are known to impede the ability of cells to properly fold and post-translationally modify secretary and transmembrane proteins in the ER, leading to production of misfolded proteins (ER stress). High levels of misfolded proteins in the ER disrupt the ER homeostasis, and then chronic ER stress may contribute to pathology of a number of diseases. Accumulating evidence suggests the role of ER stress and the unfolded protein response in the pathology of a number of neuropsychiatric diseases. Considering the role of the sigma-1 receptor as a novel molecular chaperone that regulates protein folding and degradation at the ER (3–5), the activation of sigma-1 receptor chaperone by agonists could prevent the misfolding of proteins which play a role in the pathology of neuropsychiatric diseases. The preclinical findings suggest that the activation of sigma-1 receptor chaperone by agonists, including fluvoxamine and DHEA (or DHEA-S), could produce neuroprotective effects in rodent models. Therefore, the activation of sigma-1 receptor chaperone by sigma-1 receptor agonists (e.g., fluvoxamine, fluoxetine, escitalopram, donepezil, ifenprodil) and endogenous neurosteroids (e.g., DHEA, DHEA-S, pregnenolone) might produce beneficial effects in patients with a number of neuropsychiatric diseases (Fig. 1).”
This article seems to highlight the potential of Sigma-1 receptors as well.
Have a nice night. I’ll try and share some interesting (imho) DD I ran across earlier today with the board tomorrow if time permits.
P.S.
Perhaps someone here (Falconer?) should consider creating the A2-73 page on Wikipedia. Under agonists the other drugs have a “page” attached but A2-73 is still blank. A missed to opportunity to inform others ?
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