hat
Dènyèman, yo te demontre wòl nan ATP synthase anpèchman pou neroprotection kont domaj entitotoxik nan yon etid sourit [4]. Etid la dezyèm te montre ke modèl sourit eksprime fòm imen an ATPase inhibitor faktè 1 (hif1), ki lakòz yon inhibition soutni nan ATP synthase, yo te pi plis rezistan nan lanmò neuronal apre domaj eksitotoxik. Done sa yo konsistan avèk nouvo etid J 147 poud, nan ki yon ogmantasyon nan IF1 nan sourit yo redwi aktivite a nan ATP synthase (espesyalman ATP5A) e li te neroprotective.
eng
Recently, the role of ATP synthase inhibition for neuroprotection against excitotoxic damage was demonstrated in a mouse study[4]. The second study showed that mouse models expressing the human form of mutant ATPase inhibitory factor 1 (hIF1), which causes a sustained inhibition of ATP synthase, were more resilient to neuronal death after excitotoxic damage. This data is consistent with this new J 147 powder study, in which an increase in IF1 in the mice reduced the activity of ATP synthase (specifically ATP5A) and was neuroprotective.