“A dose-dependent increase of BDNF was evident following completion of an NMES protocol, but there was no improvement in MCT performance. Gene expression in the hippocampus was increased after both AE and NMES, with IGF-1 being a signaling molecule that correlated with MCT performance in the AE conditions, but also highly correlated with VEGF-A and Klotho. “
Not sure if increasing hippocampus gene expression is a good idea. Obviously NMES increasing BDNF is very good.
It is also worth noting that NMES exhibited a dose-dependent decrease in BDNF levels, with the low NMES condition achieving a high upregulation of BDNF gene expression.
?? Decrease in BDNF?
This would also explain how an increase in BDNF in the blood stream does not correlate with changes in BDNF signaling in the hippocampus. It is also conceivable that other signaling factors in the hippocampus modulate local BDNF expression, which could lead to an uncoupling of BDNF levels from the blood.
the key molecule bridging signaling in the blood and the brain is IGF-1, with levels in both organ systems being correlated. IGF-1 was also a central signaling molecule in the hippocampus with it being correlated with VEGF-A and Klotho.
(just accidentally closed window from which I pasted this info)
I know so little about E Stim but if it can increase BDNF and Dr. Wahls says it greatly helps her MS, maybe it can help PWP.
“We conclude that brief electrical stimulation stimulates BDNF and trkB expression in regenerating motoneurons. Because electrical stimulation is known to accelerate axonal regeneration, we suggest that changes in the expression of BDNF and trkB correlate with acceleration of axonal regeneration.”
Although we are not rats, or at least not most of us, I’m hopeful this can help us.
Just in case you don't find the exact study you are looking for, the following newer review(November 2022) suggests that melatonin offers similar effects to NGF and much much more when it comes to the brain :
' Furthermore, melatonin has pleiotropic actions, which affect, for instance, the modulation of the immune and the cardiovascular systems, as well as the neuroprotection achieved by scavenging free radicals. Recent research has supported that melatonin contributes to neuronal survival, proliferation, and differentiation, such as dendritogenesis and axogenesis, and its processes are similar to those caused by Nerve Growth Factor, Brain-Derived Neurotrophic Factor, Neurotrophin-3, and Neurotrophin-4/5. Furthermore, this indolamine has apoptotic and anti-inflammatory actions in specific brain regions akin to those exerted by neurotrophic factors. This review presents evidence suggesting melatonin’s role as a neurotrophic factor, describes the signaling pathways involved in these processes, and, lastly, highlights the therapeutic implications involved. '
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