I think in sz and psychosis there are a few different hypothesis’ about how it can manifests. Some are related to the inflammation of certain pathways others to the buildup of Adrenalin. From my understanding there are two more main areas that you would want to focus on that being the dopamine and glutamate systems. You can read up on this by searching for “dopamine hypothesis schizophrenia” or look into the nmda receptor in schizophrenia and you will find information on what I am talking about.
I think the racetams are great they help in the glutamatergic systems of our brain and just about all of them protect and build the nmda receptor (which is hypothesised to be dysfunctional), some like phenylpiracetam are more specific in that it can help build the dopamine pathways more than the others. You need to take the racetams everyday and it takes about a week sometimes for them to build up and start working but there are loads of studies in dementia stroke and other cognitive problems where they show a lot of potential in repairing the brain.
Sarcosine and NAC are both supposed to be helpful. Current evidence indicates the roles of glutamatergic system in this disorder. N-acetyl cysteine (NAC) also increases extracellular glutamate.
The glutamatergic system is a key point in pathogenesis of schizophrenia. Sarcosine (N-methylglycine) is an exogenous amino acid that acts as a glycine transporter inhibitor. It modulates glutamatergic transmission by increasing glycine concentration around NMDA (N-methyl-d-aspartate) receptors. In patients with schizophrenia, the function of the glutamatergic system in the prefrontal cortex is impaired, which may promote negative and cognitive symptoms.
https://www.ncbi.nlm...ubmed/29126981/
https://www.ncbi.nlm...les/PMC4632760/
Is sarcosine the opposite of an NMDA antagonist? Therefore it would increase glutamate which in turn would give energy?