Covers many areas. Drugs and supplements include valproate, NAC, fingolimod, olexosime, pioglitazone, PUFA, Clemastine fumarate, polyphenols, and Nano-curcumin.
Neural stem cell based approaches are another possible avenue to repair WM. Gli-1 inhibitors act upon a pool of neural stem cells that express Gli1 and when Gli1 expression is repressed, these cells differentiate into oligodendrocytes (Samanta et al., 2015).
Fingolimod [FTY720, an immunodmodulator approved for use in MS (Kipp and Amor, 2012)], is believed to mimic sphingosine 1-phosphate (S1P) in vivo and a lipid mediator that acts through G protein coupled receptors and can cross the blood-brain-barrier (Chun and Hartung, 2010). Receptors for S1P are also present in the CNS. There is a listing for phase two clinical trial examining fingolimod in schizophrenia patients (STEP) active in the clinical trial registry that was due to finish recruiting patients in Dec 2017 (See Table 2). A recent study from a phase 3 trial in MS patients showed significantly less ventricular volume enlargement and less WM loss with fingolimod as compared to placebo (Gaetano et al., 2018). This raises a possibility for fingolimod to modify not only WM loss but the pathological ventricular enlargement seen in schizophrenia which would be an exciting possibility.