Distribution and Phenotype of Proliferating Cells in the Forebrain of Adult Macaque Monkeys after Transient Global Cerebral Ischemia

Restoration of Nigrostriatal Dopamine Neurons in Post-MPTP Treatment by the Novel Multifunctional Brain-Permeable Iron Chelator-Monoamine Oxidase Inhibitor Drug, M30

“…Neurogenesis in the adult brain is known to occur in three brain regions: olfactory bulbs, the forebrain rostral sub-ventricular zone (SVZ) near the striatum, the hippocampal sub-granular zone (SGZ) of the dentate gyrus (DG). The neurogenesis in these brain regions occurs following various insults (including 6-OHDA and MPTP), both spontaneously and in response to growth factors (Faiz et al 2005;Yoshimi et al 2005;Keilhoff et al 2006;Van Kampen and Eckman 2006;Lagace et al 2007;Tonchev et al 2007), although neurogenesis in the SN is controversial (Peng et al 2008).…”

“…Three hypotheses can be suggested: the first is that MPTP puts many cells on the brink of death, yet M30 prevents them from crossing the threshold to commence apoptosis or necrosis cascades; the second hypostudy is that M30 induces neurogenesis via mitosis in the SNpc; the third hypostudy is that M30 induces neurogenesis via mitosis elsewhere, and the newly formed neurons migrate to the SNpc. Neurogenesis in the adult brain is known to occur in four brain regions: olfactory bulbs, the forebrain sub-ventricular zone (SVZ) near the striatum, the hippocampal subgranular zone (SGZ), and the hippocampus, in response to various insults including MPTP and 6-OHDA), both spontaneously and growth factor-induced (Faiz et al 2005;Yoshimi et al 2005;Keilhoff et al 2006;Van Kampen and Eckman 2006;Lagace et al 2007;Tonchev et al 2007). In order to test whether mitosis is involved, thymidine analog, 5-bromo-2 0 -deoxyuridine-5 0 -monophosphate (BrdU), was administered i.p.…”

Treatment with UDP-glucose, GDNF, and memantine promotes SVZ and white matter self-repair by endogenous glial progenitor cells in neonatal rats with ischemic PVL

“…Loss of neurotrophic factor activity is a major contributor to post-ischemic degradation of the neural microenvironment (Tonchev et al, 2007). GDNF, a key neurotrophic factor required for nerve cell growth, development, and survival, has been shown to promote exogenous neural stem cell differentiation into preOLs and WM myelination (Duarte et al, 2012).…”

“…However, our laboratory has recently shown that glial progenitor-mediated self-repair of both the SVZ and WM may be limited, since recovery of fully differentiated, mature OLs was not complete (Mao et al, 2013). This may reflect an unfavorable microenvironment, including a possible shortage of appropriate neurotrophic factors (Tonchev et al, 2007). UDP-glucose (UDPG) is an endogenous agonist that may enhance endogenous self-repair potential by activation through GPR17 (Lecca et al, 2008).…”

Regulation of endogenous neural stem/progenitor cells for neural repair—factors that promote neurogenesis and gliogenesis in the normal and damaged brain

“…Some factors, such as Epo, have multiple actions, including NSPC proliferation, neuronal differentiation, and oligodendrocyte maturation, as well as being neuroprotective, which makes them particularly attractive as potential therapeutics for treatment of the damaged brain. Most of the work described above was conducted in rodents and to date little work has been performed following neural injury in brains of gyrencephalic species, such as non-human primates (Tonchev et al, 2003a,b, 2005, 2007). Sheep models are also being developed to allow such questions to be answered in a model more relevant to human brain damage (e.g., Wells et al, 2012).…”