title: An immunological basis of hyperphagia driven by GABAergic dysfunction in Prader-Willi Syndrome.
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.
authors.affiliation: Department of Surgery, Physiology and Biophysics, The University of Mississippi Medical Center, Jackson, MS 39216-4505, USA. urout@umc.edu
authors.forename: Ujjwal
authors.initials: U
authors.lastname: Rout
authors.forename: Omar A
authors.initials: OA
authors.lastname: Abdul-Rahman
authors.forename: Dirk Marcel
authors.initials: DM
authors.lastname: Dhossche
mesh_terms: D001323:Autoantibodies / Q000276:immunology*; D001921:Brain / Q000276:immunology* / Q000378:metabolism; D002884:Chromosomes, Human, Pair 15 / Q000235:genetics; D018392:Genomic Imprinting / Q000235:genetics*; D006801:Humans; D006963:Hyperphagia / Q000209:etiology / Q000276:immunology*; D009030:Mosaicism; D011218:Prader-Willi Syndrome / Q000235:genetics / Q000276:immunology*; D018079:Receptors, GABA / Q000235:genetics / Q000378:metabolism*; D014314:Trisomy / Q000235:genetics*; D024182:Uniparental Disomy / Q000235:genetics*
chemical_list: D001323:Autoantibodies; D018079:Receptors, GABA