It looks like a lot of people in this thread experienced the effects of mitochondrial dysfunction by themselves.

Here is my 2 cents based on some experience with the topic. Autoimmune manifestations may be just a normal reaction of the organism to dysfunctional cells on their way to apoptosis. Apoptosis occurs when the percentage of broken mitochondria reaches a certain threshold. So you get the inflammation. It may look like the organism attacks its own tissues by mistake - but actually there is a reason.

When the inflammation kicks in, it also affects surrounding healthy cells adding insult to the damage. You get some kind of progressing encephalopathy that eventually leads to neurodegenerative disorders.

A plausible treatment for such condition: inhibit inflammation while trying to restore the normal mitochondrial function.

A gentle way to inhibit the inflammation is to use nonsteroidal anti-inflammatory drugs such as Acetylsalicylic Acid (Aspirin).

Restoring normal mitochondrial function is considered impossible if you have an inherited mutation in mitochondrial DNA (1 in 50000 of population). However this is a pretty rare condition while the most of mitochondrial manifestations (1 in 5000 of population) are acquired from environmental factors such as poisons, drugs, infections, nutritional imbalances.

The treatment for such an acquired mitochondrial dysfunction is two-fold: 1) eliminate the initial vector (poison, infection etc. 2) reverse the damage that occurred in mitochondria.

Infections, drugs and poisons are self-explanatory. The nutritional deficit is more intricate. But in case of mitochondria, it is basically covered by the Thiamine (B1 vitamin). The only gotcha is that you won't feel the effect with supportive B1 doses like the usual 2 mg per day. You would need therapeutic doses and a more bioavailable form for that to work, like 300 mg of Benfotiamine per day.

Now once that is covered, you would just stop the progression of mitochondrial dysfunction. But that may be not enough if it went too far. You might still have the apoptosis, the associated constant inflammation and the resulting degeneration.

What you can do to rejuvenate mitochondrial function is to use substances like Nicotinamide Riboside (100 mg per day). This is an efficient B3 vitamin precursor without the typical side effects of Niacin. It restores cell respiration by playing the role of an electronic transport in aerobic glycolysis pathway (Glucose + Oxygen -> ATP) which occurs in a healthy mitochondria. Nicotinamide Riboside is the preferred form of B3 because it also plays the role of a mitochondrial growth factor which is a big win in case of mitochondrial deficit.

Now once you combine all these methods, you may be onto something. By modulating the inflammatory response you win the time to restore the mitochondria thus avoiding massive cellular apoptosis.

By gradually restoring the mitochondrial aerobic glycolysis pathway, you are gradually reducing the associated lactic acidosis which also plays a huge negative role in neurological diseases. You break the viscous cycle of anaerobic glycolysis swapping it with a normal, healthy aerobic pathway.

If the damage to the tissues and nervous system is not too substantial, it may be a full recovery given some months of therapy.