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This is a related drug "in the model of" the drug mentioned above that has not made it through the drug approval pipeline yet, probably a couple more years if not fast tracked.  I bring it up because the chart on this website kind of simply explains the mechanism of this new class.  It is literally described as ....

 

"The candidate, nelotanserin, targets the 5HT2A receptor for serotonin in cells from the central nervous system. Its activation is the basis of psychedelic drugs such as LSD. Nelotanserin does the opposite, blocking its activity to reduce hallucinations in patients with DLB and PDD."

 

 

 

http://labiotech.eu/axovant-sciences-bermuda-dementia/

 

 

Edited by Mike
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Dr Kremens: NUPLAZID is a selective serotonin inverse agonist. To understand this, you have to understand how receptors in the brain work. Many receptors in the brain are capable of initiating signals even when they are not being stimulated, even when you don’t have an agonist bound to that receptor. Signaling can occur without an agonist; that is called basal activity. If you have an agonist, that stimulates a receptor and increases the activity of that receptor. Then there are drugs called antagonists. Antagonists block the agonist, but they permit the ongoing basal activity. Then you have inverse agonists. Inverse agonists suppress basal activity. So, with NUPLAZID, you are suppressing the basal activity of some serotonin receptors in the brain. It’s thought that the effect of NUPLAZID is a result of a combination of an inverse agonist and antagonist activity at serotonin receptors.
- See more at: http://www.ajmc.com/journals/supplement/2016/understanding-the-burden-and-management-of-hallucinations/a645-article/P-4#sthash.O13qeyGg.dpuf

 

 

 

 

Edited by Mike
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I'd try it in a heartbeat.

I was thinking of trying Remeron because it antagonizes 5ht2a and is different than the typical SSRI but I'd try this first if I could get my hands on it.

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Dr Kremens: NUPLAZID is a selective serotonin inverse agonist. To understand this, you have to understand how receptors in the brain work. Many receptors in the brain are capable of initiating signals even when they are not being stimulated, even when you don’t have an agonist bound to that receptor. Signaling can occur without an agonist; that is called basal activity. If you have an agonist, that stimulates a receptor and increases the activity of that receptor. Then there are drugs called antagonists. Antagonists block the agonist, but they permit the ongoing basal activity. Then you have inverse agonists. Inverse agonists suppress basal activity. So, with NUPLAZID, you are suppressing the basal activity of some serotonin receptors in the brain. It’s thought that the effect of NUPLAZID is a result of a combination of an inverse agonist and antagonist activity at serotonin receptors.
- See more at: http://www.ajmc.com/journals/supplement/2016/understanding-the-burden-and-management-of-hallucinations/a645-article/P-4#sthash.O13qeyGg.dpuf

 

so even if your antagonizing the receptor your still activating it in a sense, antagonism returns it to it "baseline".  But if it's stuck being hyperactive so to speak, inverse agonism depresses it, it's different, a lower baseline.  The "volume" is what needs to be lowered.

 

 

Edited by Mike
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http://www.blogtalkradio.com/powerful-patient/2012/04/13/curing-the-post-lsd-syndrome

 

Ketaserin is an older hypertensive agent, also sold as a gel that is related to Nuplazid(primavanserin).  It seems to come up a lot when researching this area.  It seems like researchers are aware of its LSD blocking capabilities and effects on seretonin, however, it's only I guess shown to stop the effects of lsd when taken prior to ingestion??? Though I have never heard of anybody using it for this condition before this article was recently published.  Not sure about availability.

https://www.theverge.com/2017/1/26/14388034/lsd-acid-neuroscience-trip-meaning-research-science

Edited by Mike
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This is fascinating. Has anybody here read that book? In the descriptions I've found online he doesn't refer to it as HPPD, only "Post-LSD Syndrome." Also, the symptoms listed aren't in line with what we have. They mention depression, sleeplessness, etc., but no visual disturbances -- at least not in the summaries I read. 

Also, has anybody tried Ketaserin or Nuplazid? Both seem promising but perhaps difficult to get ahold of. Here's an interesting thread on this subject: 

http://hppdonline.com/index.php?/topic/2294-5-ht2a-antagonists-a-complete-cure-for-hppd/#comment-18303

Lastly, did anybody else have a profound sense of meaning shortly after getting HPPD? I haven't thought much of it until reading all this stuff, but I remember in the first few weeks after getting HPPD having an absolutely revelatory sense of understanding about the world and how life was only worth living when there was meaning involved -- essentially all the stuff you're supposed to have happen while tripping, except this was weeks later. Clearly there was something going on with those same receptors that induce meaning into the world, I just don't know what exactly. 

Edited by K.B.Fante
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This is a drug that dasitmane and I sort of was looking at in 2013 i think. 

dasitmane was always saying ht2a inverse agonists.  So I found Acadia.  I bought the stock at $2.60 at dasitmane's advice.  A family member thought I was crazy so I didn't buy as much as I wanted.  Uggh.   We need someone to get on it and see.  Right now I think it is only for Parkinsonian psychosis but soon will be an add-on for schizophrenia I believe. 

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Maybe the drug company will get greedy and push to have it as an add on for MDD and it'll be the next Abilify handed out like candy. 

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For what it's worth, I contacted the authors of the recent North Carolina study about whether they think HPPD could be a result of a permanent sealing of the lid on the seratonin receptor and one of them said he thinks its highly unlikely. In fact, he specifically said he thinks there's no way it's even possible. Instead, he suggested the visual cortex could have become "sensitized" given our visual disturbances and the fact this area of the brain has a high number of 5-HT2A receptors. 

He sorta sounded like he was just spitballing, but I guess it's something. Still doesn't tell us much. 

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8 hours ago, Mike said:

Also kind of wonder about the low dose of Zyprexa or antipsych meds the one doctor had success with, whether that actually holds up or if they act differently when not causing so much stimulation.

I'm getting on 2.5 mg Zyprexa soon. Probably this week.

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Interesting tidbit about Remeron:

"A case report has been published in which mirtazapine reduced visual hallucinations in a patient with Parkinson's disease psychosis (PDP).[42]This is in alignment with recent findings that inverse agonists at the 5-HT2Areceptors are efficacious in attenuating the symptoms of Parkinson's disease psychosis. As is supported by the common practice of prescribing low-dose quetiapine and clozapine for PDP-doses too low to antagonise the D2receptor, but sufficiently high doses to inversely agonise the 5-HT2Areceptors."

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