An immunological basis of hyperphagia driven by GABAergic dysfunction in Prader-Willi Syndrome.
Academic Article
Overview
abstract
Impaired immune function is increasingly seen as a core element of various neurological, psychiatric, and developmental disorders but has not yet been investigated in subjects with Prader-Willi Syndrome. We hypothesize that the emergence and the progression of PWS may be regulated by immune dysfunction involving auto-antibodies and miRNA driven by GABAergic dysfunction. Future research testing this hypothesis is discussed.
