Retinoic acid induces neurogenesis by activating both retinoic acid receptors (RAR) and peroxisome proliferator-activated receptor β/δ (PPARβ/δ)

You have to ask your doctor how this can be translated into a therapy protocol.
http://www.jbc.org/content/early/2012/10/26/jbc.M112.410381.short

Abstract

Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARβ/δ and their respective cognate lipid binding proteins CRABP-II and FABP5. RA induces neuronal differentiation but the contributions of the two transcriptional pathways of the hormone to the process are unknown. Here we show that RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARβ/δ path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. In contrast with its inhibitory activity in early steps of neurogenesis, the FABP5/PPARβ/δ path promotes differentiation of neuronal progenitors to mature neurons, an activity mediated in part by the PPARβ/δ target gene PDK1. Hence, RA-induced neuronal differentiation is mediated through RAR in early stages and through PPARβ/δ in late stages of the process. The switch in RA signaling is accomplished by a transient upregulation of RARβ concomitantly with a transient increase in the CRABP-II/FABP5 ratio at early stages of differentiation. In accordance with these conclusions, hippocampi of FABP5-null mice display excess accumulation of neuronal progenitor cells and a deficit in mature neurons vs. wild-type animals.