In Vivo Expression of Reprogramming Factor OCT4 Ameliorates Myelination Deficits and Induces Striatal Neuroprotection in Huntington’s Disease

White matter atrophy has been shown to precede the massive loss of striatal GABAergic neurons in Huntington’s disease (HD). This study investigated effects vivo expression reprogramming factor octamer-binding transcription 4 (OCT4) on neural stem cell (NSC) niche activation subventricular zone (SVZ) and induction fate specific microenvironment HD. R6/2 mice randomly received adeno-associated virus 9 (AAV9)-OCT4, AAV9-Null, or phosphate-buffered saline into both lateral ventricles at weeks age. The AAV9-OCT4 group displayed significantly improved behavioral performance compared control groups. Following treatment, number newly generated NSCs oligodendrocyte progenitor cells (OPCs) increased SVZ, OPC-related genes glial cell-derived neurotrophic (GDNF) increased. Further, amelioration myelination deficits corpus callosum was observed through electron microscopy magnetic resonance imaging, DARPP32+ group. These results suggest that situ OCT4 SVZ induces OPC proliferation, thereby attenuating deficits. Particularly, GDNF released by OPCs seems induce neuroprotection HD, which explains improvement overexpressing OCT4.