Research has shown that mitochondria protecting agents could offer theraputic benefits in ALS. I am looking for suggestions on which ones, already used in humans, would be good candidates for further research?
Dear Henry!
Please You look at these articles:
Article Potential Therapeutic Benefits of Strategies Directed to Mitochondria
Table 1.
Strategies for Effective Drug Delivery into the Mitochondrial Matrix
V. Mitochondrial ROS Scavenging and Its Potential Therapeutic Value
Article The Role of Mitochondria in Amyotrophic Lateral Sclerosis
Table 1. Impact of ALS-associated genes on mitochondrial function. Pathogenic variants of proteins implicated in ALS have been linked to altered mitochondrial function (Ref.
Neuron-based high-content assay and screen for CNS active mitotherapeutics
https://advances.sciencemag.org/content/6/2/eaaw8702 (attached)
L-carnitine supplementation suppresses the onset of neuromusclar degeneration and increases the life span in mice ALS model with SOD-1 mutation (Kira Y. et al Brain Res 2006; 1070: 206-14.). Also there is a clinical trial of acethyl-L-carnitine to ALS (Beghi E. Amyotroph Lateral Scler Frontotemporal Degener
. 2013 Sep;14(5-6):397-405. )
Additional information for your question.@@
L-carnitine has the anti-wasting effects in various basic and clinical settings (Ringseis R. Eur J Nutr 2013; 52: 1421-42.). Also the potential antioxidant activity of -carnitine should be applied for the inherited neurometabolic disorders (Ribas GS. Gene 2014; 533; 469-76.). The mechanism of the antioxidant effects is related to Nrf-2 activation which induce antioxidant enzymes and cell protecting proteins ( Calabrese V. Biochim Biophys Acta 2012; 1822: 753-83.). If you needs more information, please contact to me.
Hi Henry,
My reply may be a bit off-subject, but it's not off-target. If you're looking for an Nrf2 activator, the most studied is sulforaphane. It is not a drug, but a natural isothiocyanate that can easily made from Broccoli seeds. I have been using it to reduce oxidative stress in PD. Recently, a small group of PD patients used it in a self-supervised experiment based on a protocol I established. Of course it was not a full (placebo - double blinded) trial, just an experiment to try to identify which symptoms might be sensitive to sulforaphane. The results were quite specific, non-motor symptoms of PD responded rapidly and strongly whereas motor symptoms did not. More specifically, the most responsive symptoms were energy related (fatigue, sleep quality, lack of motivation) suggesting a direct connection to resolving oxidative stress in mitochondria.
The experiment is described here (mostly for non scientists) and gives a link to the results.
https://patientresearcher.wordpress.com/2021/01/15/resetting-the-redox-balance-to-slow-parkinsons-disease/
The scientific basis is here;
Preprint Role of the transcription factor Nrf2 and Redox Balance in P...
I hope you find this useful,
Albert
I think the best focus in ALS is not on mitochondria but lysosome.
https://www.researchgate.net/project/Exploring-novel-treatment-for-amyotrophic-lateral-sclerosis
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