nefiracetam for shizophrenia

[MeDieViL]

I personally found this racetam extremely effective for positive symptions induced by amphetamine; it even completely reversed semi psychosis multiple tymes.

I compiled all study's behind its MAO on my blog; shizophrenia is mainly caused by glutamate hypoactivity and indeed its mostly glutaminergic in action.
http://noveltreatments.blogspot.co.uk/2012/04/pharmacology-and-therapeutic-potential.html

I was predromal shizophrenic (i say was as it appears i completely reversed this state even much better i went much improved to how ive been my whole life but ill make a separate thread about this later) however it should also work against paranoia or semi psychosis for normal individuals i beleive.

 

[tamarinds]

Im guessing you havnt read this:

http://www.longecity.org/forum/topic/54506-nefiracetam-another-reason-to-avoid-prolonged-usage/

 

[_Olon_]

I have schizophrenia with almost exclusively cognitive and negative symptoms and what helps me most is anti-glutamate medication. Currently I have good success with lamotrigine and quercetin.
In the nineties effectiveness of AMPA receptor antagonists in the PCP-induced hyperlocomotion model has been shown, something that seems to have been forgotten.
http://www.ncbi.nlm.nih.gov/pubmed?term=AMPA hyperlocomotion
I am curious to see what perampanel will do (an AMPA receptor negative allosteric modulator that will come out probably this year).
Strangely increasing excitability by blocking potassium channels seems to be effective as well.
http://www.freepatentsonline.com/y2010/0310681.html
I wonder what will happen if one combined the two. Will they cancel out each other?

 

[MeDieViL]

Lamotrigine is pro glutaminergic in some ways wich is why it helps shizophrenia; ill go deeper in this when ive got more time.

 

[_Olon_]

Untreated schizophrenics have elevated glutamate in the prefrontal cortex, whereas treated schizophrenics don't differ from healthy people.
http://www.ncbi.nlm.nih.gov/pubmed/22213769
http://www.ncbi.nlm.nih.gov/pubmed/20970118
Glx in treated schizophrenics positively correlates with cognitive functioning, which implies that some schizophrenics suffer from too strong reduction of glutamate release by their medication.
Do you still take phenibut?

 

[MeDieViL]

Indeed there's excessive glutamate in the pfc.

Yes i do but what i take lately is not related to shizophrenia; i feel well improved enough (i dont even need gabaergics with stims anymore at all; they never cause even something related to positive symptions; i do have a blunted response to stims (shizo's have a hyperresponse; however when stabilised a hypoactive response).
Its just negatives really i still suffer from (anhedonia; adhd; ocd; SA) wich i take stimulants for; i was taking phenibut as it besides stims was the only thing helping my anhedonia but now ive got stims back i plan to stop taking it with the use of diazepam for a week.

I never noticed tolerance to phenibut wich could perhaps be because of my old shizo brain; i used it weeks daily without tolerance im no longer immume to withdrawals anymore tough like the past.

There's alot of excitoxiticy implicated in shizo wich is why both glutamate agonists and antagonists can help; i used to have alot of succes with memantine but going the other way thats how i got above this desease.

Most shizo's id advice to start with pregnenolone as it increases myelenation; repairs axons and is very neurotrophic exactly the way a shizophrenic would need it to reverse alot of the neurodegeneration.
Also chronic social exposure is crucial for recovery.

 

[MeDieViL]

Im guessing you havnt read this:

http://www.longecity.org/forum/topic/54506-nefiracetam-another-reason-to-avoid-prolonged-usage/

That thread is stupid; just because it increases gaba its dangerous? gimme a break endogenious gaba must be dangerous then as well.

Wheter the testicle toxiticy apply's to humans is debatable; in favor are the post stroke apathy trials showing it appears to be safe for humans but caution is allways adviced. Staying under 100mg a dose is a good idea.

 

[MeDieViL]

Untreated schizophrenics have elevated glutamate in the prefrontal cortex, whereas treated schizophrenics don't differ from healthy people.
http://www.ncbi.nlm.nih.gov/pubmed/22213769
http://www.ncbi.nlm.nih.gov/pubmed/20970118
Glx in treated schizophrenics positively correlates with cognitive functioning, which implies that some schizophrenics suffer from too strong reduction of glutamate release by their medication.
Do you still take phenibut?

Only in the pfc there's too much glutamate; in the rest of the brain there's hypoactivity of the whole glutamate system.

 

[_Olon_]

I ask for phenibut because stimulation of presynaptic GABA B receptors lead to a decreased glutamate release.

 

[MeDieViL]

I ask for phenibut because stimulation of presynaptic GABA B receptors lead to a decreased glutamate release.

I beleive it actually induces glutamate release somehow; its definatly differend from presynaptic doses of baclofen and feels very simular to GHB.

But thats just speculation.

 

[_Olon_]

I found an interesting article.
http://www.ncbi.nlm.nih.gov/pubmed/9286612
They tested two AMPA positive allosteric modulators and one of them was indeed effective in BOTH amphetamine and PCP induced hyperlocomotion model. The other one was not effective in BOTH. It's just two of them, but hard to believe that there is one that does stim potentiation (non-effectiveness in the amphetamine model) and schizophrenia treatment (effectiveness in the PCP model) at the same time. Better stay away from nootropics that do stim potentiation.

 

[DexterMeth]

Better stay away from nootropics that do stim potentiation.

Can you please clarify?

 

[_Olon_]

Can you please clarify?

As I already wrote it's just an assumption, but the finding that one AMPA receptor positive allosteric modulator is effective both in the amphetamine and PCP model and the other in none of them makes me believe that any AMPA positive allosteric modulator that is suitable for schizophrenia treatment will block stim effects (effectiveness in the amphetamine model).
Maybe with an mGlu2 receptor agonist plus L-dopa one will be able to have stim effects plus antipsychotic activity.
http://www.ncbi.nlm.nih.gov/pubmed/20585759

 

[bben]

Only in the pfc there's too much glutamate; in the rest of the brain there's hypoactivity of the whole glutamate system.

glutamate acts on nmda to inhibit dopamine in the limbic system. By blocking nmda, dopamine is released from tonic inhibition and you get psychosis. This is combined with the PFC glutamate release caused by nmda blockade, which causes its own issues.