There is a lot of theories but these are the main ones. Reality is likely a mix of all these theories.
Yes, I love medicine. I did study some in neuro and psy university courses. No, I am not a dr.
Genetic theory
Dopamine hyperactivity (Positive
symptoms)
Serotonin imbalance (Positive
symptoms)
Glutamate (NMDA and AMPA receptors)
hypoactivity
(Negative and Cognitive symptoms)
Hypofrontality (Negative symptoms)
Parietal lobe cortex brain tissue loss (Positive
and Cognitive symptoms)
Neurodevelopment abnormalities
Neural connections misconnection and weak
connections.
Incorrect neural connection pruning (shaping)
or failure
(Newest) Acetylcholine (Muscarinic
and Nicotinic receptors) hypoactivity (New AP
Xanomeline Phase 3 trials)
Do you think they will find a full cure for SZ one day?
I can’t wait to try Xanomeline in a couple of years.
There’s also one about histamine receptors, which is something my new antipsychotic, Vraylar, targets. It makes sense because I have very high levels of histamine, and when I got off my antihistamine, I had my break.
I’m also very interested into the science of both schizophrenia and how medication works. So, while I’m off of school for a few weeks, I’ll research more into the science.
It hasn’t begun to work yet, so I’m still going off of risperdal. But I’d imagine that my negative and cognitive symptoms will improve as they’re something that I’ve been struggling with recently, especially lack of motivation. I’m going to be completely on Vraylar in about a month when I can lower my risperdal dose.
Wikipedia says its good for cognitive symptoms. Nothing about negative symptoms. Where did you read that it acts on histamine? They only say its different than other AP because it reduces dopamine when dopamine is high and increases dopamine when dopamine is low. Its a modulator, not an antagonist. Other APs except Abilify completely block dopamine all the time.