Inosine and neural growth
Posted: Wed Feb 06, 2013 6:31 am
Hi,
I'm surprised to report that there may be more to Inosine than just being the precursor to Uric acid.
I learned from this board that uric acid is an antioxidant, usually low in people with MS and helpful to protect against bladder infections etc.
I started taking Inosine as a way to jump start my uric acid.
Then I took the word Inosine as a search term to pub med central and discovered that the stroke doctors think this stuff is good for the regrowth of axons.
Here is a sample of what I found.
I'm off to enjoy a 12 hour work day, so I'll check in later. Hopefully this is helpful.
Promoting axonal rewiring to improve outcome after stroke
Neurobiol Dis. 2010 February; 37(2): 259.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818530/
One molecule that enhances axon growth and improves outcome in a rat stroke model is inosine. Inosine is a naturally occurring purine nucleoside that gets transported across the cell membrane and activates Mst3b, a protein kinase that regulates the cell-signaling pathway through which trophic factors induce axon growth (Irwin et al., 2006; Lorber et al., 2009). Additional benefits of inosine after brain injury include its anti-inflammatory effects (Hasko et al., 2004), its ability to suppress glutamate-induced neural excitation (Shen et al., 2005), and the ability of its metabolite, uric acid, to protect proteins from peroxynitrite-induced damage (Scott et al., 2005, 2002). Following unilateral cortical damage, inosine enhances the ability of undamaged neurons to extend axon collaterals into areas that have lost their normal innervation; this growth is accompanied by improved performance with the limb contralateral to the stroke (Chen et al., 2002; Zai et al., 2009). As illustrated in Fig. 2, sustained delivery of inosine after injury to the caudal forelimb area in one hemisphere increases the ability of pyramidal cells on the undamaged side of the brain to extend axon collaterals and form synapses on the denervated side of the spinal cord (Fig. 2a-c). After 4 weeks, animals treated with inosine are far superior to saline-treated animals in their ability to use the paw contralateral to the damaged hemisphere in a test requiring fine motor control (Fig. 2d: Zai et al., 2009). Similar results have been obtained in studies using a closed-head injury model (Smith et al., 2007). At the molecular level, stroke on one side of the brain causes layer 5 pyramidal cells in the opposite hemisphere to undergo many changes in gene expression, presumably related to denervation and stress. Inosine reverses many of these changes, while at the same time inducing the expression of genes related to axon growth and the complement cascade (Zai et al., 2009). The latter changes may be of particular significance in view of recent studies linking the complement cascade to synaptic reorganization (Stevens et al., 2007).
Figure 2
Inosine enhances axonal rewiring and augments functional recovery in an animal model of stroke
I'm surprised to report that there may be more to Inosine than just being the precursor to Uric acid.
I learned from this board that uric acid is an antioxidant, usually low in people with MS and helpful to protect against bladder infections etc.
I started taking Inosine as a way to jump start my uric acid.
Then I took the word Inosine as a search term to pub med central and discovered that the stroke doctors think this stuff is good for the regrowth of axons.
Here is a sample of what I found.
I'm off to enjoy a 12 hour work day, so I'll check in later. Hopefully this is helpful.
Promoting axonal rewiring to improve outcome after stroke
Neurobiol Dis. 2010 February; 37(2): 259.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818530/
One molecule that enhances axon growth and improves outcome in a rat stroke model is inosine. Inosine is a naturally occurring purine nucleoside that gets transported across the cell membrane and activates Mst3b, a protein kinase that regulates the cell-signaling pathway through which trophic factors induce axon growth (Irwin et al., 2006; Lorber et al., 2009). Additional benefits of inosine after brain injury include its anti-inflammatory effects (Hasko et al., 2004), its ability to suppress glutamate-induced neural excitation (Shen et al., 2005), and the ability of its metabolite, uric acid, to protect proteins from peroxynitrite-induced damage (Scott et al., 2005, 2002). Following unilateral cortical damage, inosine enhances the ability of undamaged neurons to extend axon collaterals into areas that have lost their normal innervation; this growth is accompanied by improved performance with the limb contralateral to the stroke (Chen et al., 2002; Zai et al., 2009). As illustrated in Fig. 2, sustained delivery of inosine after injury to the caudal forelimb area in one hemisphere increases the ability of pyramidal cells on the undamaged side of the brain to extend axon collaterals and form synapses on the denervated side of the spinal cord (Fig. 2a-c). After 4 weeks, animals treated with inosine are far superior to saline-treated animals in their ability to use the paw contralateral to the damaged hemisphere in a test requiring fine motor control (Fig. 2d: Zai et al., 2009). Similar results have been obtained in studies using a closed-head injury model (Smith et al., 2007). At the molecular level, stroke on one side of the brain causes layer 5 pyramidal cells in the opposite hemisphere to undergo many changes in gene expression, presumably related to denervation and stress. Inosine reverses many of these changes, while at the same time inducing the expression of genes related to axon growth and the complement cascade (Zai et al., 2009). The latter changes may be of particular significance in view of recent studies linking the complement cascade to synaptic reorganization (Stevens et al., 2007).
Figure 2
Inosine enhances axonal rewiring and augments functional recovery in an animal model of stroke
