(−)-d-Deprenyl attenuates apoptosis in experimental brain ischaemia

(−)Deprenyl-N-oxide, a (−)deprenyl metabolite, is cytoprotective after hypoxic injury in PC12 cells, or after transient brain ischemia in gerbils

“…It was also demonstrated that (−)deprenyl reduces H 2 O 2 production in the course of dopamine metabolism [1]. Its neuroprotective effect was documented in the permanent MCA occlusion model in rats [2,3]. (−)Deprenyl maintains mitochondrial membrane integrity ΔY m , and reduces the level of ROS, as we reported previously [4,5].…”

Brain Plasticity Following Ischemia: Effect of Estrogen and Other Cerebroprotective Drugs

“…This post-ischemic axonal sprouting establishes new neuronal connection pattern for the damaged brain areas (Carmichael, 2003). Axonal sprouting after different central nervous system injuries can be detected by using growth-associated protein-43 (GAP-43) as it is a marker of regeneration in the adulthood (Benowitz and Routtenberg, 1987;Benowitz and Perrone-Bizzozero, 1991;Simon et al, 2001;Wappler et al, 2011b). During brain development GAP-43 is highly associated with the elongating axons (Benowitz and Routtenberg, 1987;Benowitz and Perrone-Bizzozero, 1991), which becomes less concentrated proximal to the cell soma while the axon is growing, but stays in the growth cone (Benowitz and Perrone-Bizzozero, 1991).…”

“…These data indicate increased that anti-apoptotic gene expression itself can contribute to the amelioration of brain plasticity and its effect might be modified under different stress conditions. Several drugs that are known to be cytoprotective against cerebral ischemia, such as (-)-D-Deprenyl (Simon et al, 2001), and 17-estradiol , also participate in brain regeneration. Although both have anti-apoptotic effect, (-)-D-Deprenyl increases GAP-43 expression whereas 17-estradiol treatment does not, suggesting that similar pathways may mediate enhanced regeneration through different intracellular signaling (Simon et al, 2001;Szilagyi et al, 2009; both in vitro and in vivo.…”

“…Several drugs that are known to be cytoprotective against cerebral ischemia, such as (-)-D-Deprenyl (Simon et al, 2001), and 17-estradiol , also participate in brain regeneration. Although both have anti-apoptotic effect, (-)-D-Deprenyl increases GAP-43 expression whereas 17-estradiol treatment does not, suggesting that similar pathways may mediate enhanced regeneration through different intracellular signaling (Simon et al, 2001;Szilagyi et al, 2009; both in vitro and in vivo. This is supported by btudies on other cerebroprotective drugs, such as erythropoietin (EPO) (Iwai et al, 2010), statins (Céspedes-Rubio et al, 2010), amphetamine (Liu et al, 2011), melatonin González-Burgos et al, 2007), and different spices (Kannappan et al, 2011), where different ways of imporoved brain plasticity was described.…”

Combination effect ofp-hydroxybenzyl alcohol and mesenchymal stem cells on the recovery of brain damage in a rat model of brain ischemia

“…It results from a transient or permanent reduction in cerebral blood flow in most cases, caused by the occlusion of a cerebral artery either by an embolus or by local thrombosis (Dirnagl et al 1999). The primary aim of therapeutic intervention is to reduce the volume of brain damage and thus to minimize neurological impairment (Simon et al 2001). Ischemic injury in the brain results in neuronal cell death, with characteristics of both necrosis and apoptosis (Lipton 1999;Chen et al 2001;Graham & Chen 2001).…”