Do note mitochondria are responsible for our cells’ energy production. Aside from a genetic defect, mitochondrial functions can be helped by mitophagy (getting rid of dysfunctional mitochondria) and reducing inflammation.
Two recent supplements have been found to directly impact these mitochondrial issues. Urolithin A induces mitophagy to clear out bad mitochondria even from cells that are senescent. GlyNAC (equal parts amino acids glycine and cysteine (NAC)) allows glutathione to be again produced within cells and mitochondria, which brings down most intracellular inflammation. Either can bring back cells that had dysfunction, due to either issue.
An antioxidant/amino acid that greatly helps mitochondria from getting damaged is ergothioneine. We can't make it, but it is almost exclusively available from mushrooms, with oyster mushrooms particularly high in it. This antioxidant uses its own custom, pre-existing ion channel to slide into cells’ mitochondria. Our mitochondria are capable of regenerating this for over three weeks’ worth of use. In essence, our bodies were made to get ergothioneine into every individual cell.
Finally, another cellular-level antioxidant, SOD, is dependent on the amino acid taurine. Supplementing taurine has been shown to increase SOD over 20%.
I have previously posted studies on each of these.
Interesting post, you obviously have more than a passing interest in such matters.
Might I ask what your field is?
I have some familiarity with ALS as I have designed FES and NMMS equipment that can be of assistance to sufferers... in a crude way, unfortunately...
From “Antioxidants in Central Nervous System Diseases: Preclinical Promise and Translational Challenges:”
Very early work by Perry's group found that four different antioxidants (α-tocopherol, β-carotene, N-acetyl cysteine or ascorbic acid) partially protected C57-black mice against the acute neurotoxicity of MPTP. Subsequent work by the same group found that neither α-tocopherol nor β-carotene in massive doses offered any protection against MPTP in a primate (marmoset) model. Independent, but roughly contemporaneous, studies reported that α-tocopherol, ascorbate, dimethyl sulfoxide, cysteamine or sodium selenite offered no protection against MPTP in the mouse model. Thus, most studies investigating the canonical antioxidant vitamin E have been very negative with respect to observations of protective effects in the MPTP model.
Other antioxidants besides α-tocopherol have met with greater success in treating preclinical models of PD. Table 3 summarizes the various antioxidants studied for PD in the important animal studies/clinical trials. Among antioxidants previously discussed in this review, SOD-mimicking metalloporphyrins (AEOL11207, EUK-134, EUK-189) and epigallocatechin-gallate effectively antagonize MPTP dopaminergic toxicity in mice. The synthetic nitrone-based free radical trap α-phenyl-N-tert-butyl nitrone (PBN) reproducibly protects against MPTP, though notably it does so without diminishing the level of salicylate-trappable hydroxyl radicals generated through the MPTP paradigm.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669703/
This is effectively saying only N-acetyl cysteine (NAC), green tea extract EGCG, and SOD-like antioxidants were found to help more than just a small amount against ALS.
The NAC would have likely helped make glutathione (we make more with glycine also added) and taurine could help make SOD. The EGCG is just icing on the cake, but it can bump up liver enzymes, unlike the amino acids.
It is, at least, interesting and promising. If I had such conditions, I'd be taking these (I have been taking them for a short while, regardless, without issue).