What you'd want to look at is cannabidiol with its inverse agonism of the orphan receptor GPR55 as far as promotion of neurogenesis. Or, for real, cerebrolysin though I think the CNTF in commercial cerebrolysin as a contaminant from the porcine brains it is derived from requires further purification to use, to remove NGF for transocular usage and BDNF for vaccination usage. NGF which would otherwise cause cancer and reduce the cerebrolysin to pure BDNF which is the active in some vitamin injections as well as the end target of specific adenovirus associated vectors which enhance BDNF promotion in vaccines. TrkB activity is also found in vitamins with 7,8-dihydroxyflavone with direct TrkB agonism. BDNF is what promotes growth cone formation through it's active trafficking along the f-actin within neurons to allow the tropomyosin receptor kinase b to promote growth cone formation through shady unseen pathways.

NGF is also similarly trafficked along filamentous actin. Some use NGF in eyedrops and report enhanced visual acuity and regulation of sleep-wake cycle due to stimulation of neurogenesis in the suprachiasmatic nucleus. Finally, some report that ion activity is essential to the function of the neurogenetic cycles especially with magnesium and zinc which are pore blockers at NMDA, but only for resting potentials unlike lead which is a more efficient pore blocker and blocks at all potentials. Rubidium would presumably lie somewhere in between and block at some potentials. All but lead are sometimes used therapeutically, rubidium as Rubidinorm in italy.