This is interesting… Has anyone ever tried the supplement MitoQ? Seems like it might be something to try…
On a positive note, the mice’s fluctuations in miR-137 and COX6A2 levels could be corrected by administering an antioxidant compound called MitoQ. Upon receiving MitoQ, parvalbumin neurons in the prefrontal cortex of the animals regained their function.
Might be the same issue as Amyloban 3399 vs regular Lion’s Mane supplements. The Amyloban seems to pack a wallop the other supplements don’t. I sure wish they worked as I’d save a bundle. A month off of the good stuff and my positive symptoms and nerve pain really start ramping back up. Betting the MitoQ gives you more bang, but requires more bucks.
Trehalose is a sugar mainly found in bugs and junk food. It has mitochondrial benefits. I remembered it when I read your post because it’s been seen to be protective in a number of neurological disorders.
What do you guys think of Trehalose as a different angle on SCZ mitochondrial dysfunction?
"induction of autophagy in aged mice using the disaccharide trehalose found in plants and fungi led to functional myelin clearance and disease remission"
https://www.nature.com/articles/cddis2017453 "Trehalose ameliorates oxidative stress-mediated mitochondrial dysfunction and ER stress via selective autophagy stimulation and autophagic flux restoration in osteoarthritis development"
Trehalose is a sugar which, on a cellular level, appears to have therapeutic mechanisms by regulating protein unfolding. Practically, its low oral absorption in its intact form paired with rapid digestion may preclude any benefits of oral intake.
By analysing the blood of patients diagnosed with psychosis, Do’s group was able to determine the levels of miR137 and COX6A2 in the brain. Using these two molecules as biomarkers, they succeeded in demonstrating that among the great heterogeneity of schizophrenia patients there are two major and distinct groups, those with and those without mitochondrial impairments. In addition, the mitochondrial abnormalities are associated with cognitive impairments and the corresponding clinical symptoms: loss of autonomy and reduced social skills. “Patients suffering from a mitochondrial deficiency have more severe clinical symptoms than others”, explains Inès Khadimallah.
The study thus revealed two biomarkers that would make it possible to accurately select patients who are likely to benefit from a treatment targeting the deregulation of cerebral mitochondria. “Our work paves the way for a precise diagnosis and an early, individualised treatment for people with a high clinical risk”, concludes Kim Do.
So it sounds like it’s going to be one of those things that only benefits specific people. But that’s still great if they can relatively easily test for who will benefit.