Bit of an idea for possible CURE. Has some weight to it.

[Fawkinchit]

New study shows 70% proliferation of neural progenitor cells. Which basically means neuronal stem cells that are limited to the amount they can replicate. The study did not however show if there was any replacement of lost neurons. Also, anyone reading this, please realize that harmine is hallucinogenic and proven in one of the studies posted already in this thread to kill neurons, so please to not take harmine on a random chance that it might improve your hppd, as of right now it would most likely just make it worse. 

https://www.sciencedaily.com/releases/2016/12/161207124115.htm

Human neural progenitors exposed to harmine, an alkaloid presented at the psychotropic plant decoction ayahuasca, led to a 70 percent increase in proliferation of these cells. The effect of generating new human neural cells involves the inhibition of DYRK1A, a gene that is over activated in patients with Down syndrome and Alzheimer's Disease. Thus harmine could have a potential neurogenesis role and possibly a therapeutic one over cognitive deficits.

 

 

Ayahuasca is a beverage that has been used for centuries by Native South-Americans. Studies suggest that it exhibits anxiolytic and antidepressant effects in humans. One of the main substances present in the beverage is harmine, a beta-carboline which potential therapeutic effects for depression has been recently described in mice.

 

"It has been shown in rodents that antidepressant medication acts by inducing neurogenesis. So we decided to test if harmine, an alkaloid with the highest concentration in the psychotropic plant decoction ayahuasca, would trigger neurogenesis in human neural cells," said Vanja Dakic, PhD student and one of the authors in the study.

In order to elucidate these effects, researchers from the D'Or Institute for Research and Education (IDOR) and the Institute of Biomedical Sciences at the Federal University of Rio de Janeiro (ICB-UFRJ) exposed human neural progenitors to this beta-carboline. After four days, harmine led to a 70% increase in proliferation of human neural progenitor cells.

Researchers were also able to identify how the human neural cells respond to harmine. The described effect involves the inhibition of DYRK1A, which is located on chromosome 21 and is over activated in patients with Down syndrome and Alzheimer's Disease.

"Our results demonstrate that harmine is able to generate new human neural cells, similarly to the effects of classical antidepressant drugs, which frequently are followed by diverse side effects. Moreover, the observation that harmine inhibits DYRK1A in neural cells allows us to speculate about future studies to test its potential therapeutic role over cognitive deficits observed in Down syndrome and neurodegenerative diseases," suggests Stevens Rehen, researcher from IDOR and ICB-UFRJ.

 

Edited April 10, 2017 by dasitmane

[Fawkinchit]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181663/

Just going to leave this here for future reading. 

I am finding a lot of information saying that hallucinogens do not cause neuronal loss, but I'm still doubtful. 

Found in the article posted

Recent electrophysiological studies have produced new evidence that both psychedelic hallucinogens and NMDA antagonists activate the serotonergic system and enhance glutamatergic transmission via non-NMDA receptors in the frontal cortex.^93,94 Whether this common mechanism contributes to the higher-level cognitive, perceptual, and affective effects of serotonergic hallucinogen and NMDA antagonists warrants further investigation.⁴⁰

So excitotoxicity via glutamate could be the culprit. 

Enjoy some music guys. Fast forward to 1:19:30

[

Edited April 11, 2017 by dasitmane

[mgrade]

Hey, 

 

 I have been feeling really down. 

I have, sort of, accepted I will always have this tremendous panic, anxiety, and depression.   And I find in my daily life these things are often reinforced by certain things. 

I don't have any advice to give.  

I am sort of watching my life go by.   

It is not the worst thing in the world, I suppose.

But a series of difficult incidences have left me very affected. 

 

It's the same sort of emotive/limbic reaction I have had in the past. Except I am older.  I deal with it a bit differently. 

Mortality seems so real now.  

 

I will probably never be able to function 'normally' in society ever.

 

Oddly, I see my life playing out to my death.   It might be a while or not.  I don't know. 

What I do know is that I feel like I have been forced not to care.   No one person in particular is forcing me not to care; I think time is forcing me not to care.  

 

In my life, that is the only thing I really am ashamed of is being forced not to care.   Because I am a compassionate person.  But none of it matters because I think compassion is too much of an abstract idea for people.  

 

I have made loads of mistakes.   But the core of me is good. 

 

I wish you all great love!  

[This makes me think of this Richard Alpert speech where he says Suffering is caused by the want for permanence.  Well, I am definitely paraphrasing, I am not sure exactly what he said, but I think my feelings are going beyond that, in not a great way, at this moment.   This is a bad place I am in, permanence or not.]

 

 

Edited May 1, 2017 by mgrade

[mgrade]

Prior to New York Times Magazine, May 7th 2017 edition, without any knowledge, this is what I posted on social media:  

 

 

[mgrade]

[mgrade]

Canada and Australia, the UK, under the devices of the United Kingdom, have taken on Mexico, Latin America, South America, the Caribbean, etc. as a means to the               'Global Laudromat'.    

 

Drugs, Smuggling, Human Trafficking, Money Laundering, etc. 

 

[Note: likely involved in Russian money laundering as well].  

Scotiabank, HSBC, etc.

 

Edited May 9, 2017 by mgrade

[Fawkinchit]

Has anyone by chance found any information as to what may be the most definitive cause for this condition.

 

The only 3 specific things that I can think are

Neuronal excitotoxic apoptosis

Chemical embedment in the synapses that cant be broken down

Or some altercation of DNA changing neuronal function

[mgrade]

Frying your brain with dissociative or hallucinogenic compounds ...

 

Consciousness is a complex thing.  You start bungling with the circuitry of the brain, your collective sensory system and cognition get all messed up.  

 

I'd say if you get this from a dissociative drug, it tends to be more NMDA/G related.  LSD: serotonin.  Amphetamine/MDMA: Dopamine 

 

 

 

[mgrade]

Airbourne Chaff

 

https://en.m.wikipedia.org/wiki/Chaff_(countermeasure)

http://m.lasvegassun.com/news/1997/aug/04/effects-of-chaff-still-a-mystery/ 

http://aip.scitation.org/doi/10.1063/1.3606449 

http://home.earthlink.net/~joannefstruve/_wsn/page3.html

[mgrade]

Fenugreek Seeds (newly germinated)

https://www.researchgate.net/publication/311088104_Fenugreek_Seed_Powder_Nullified_Aluminium_Chloride_Induced_Memory_Loss_Biochemical_Changes_Ab_Burden_and_Apoptosis_via_Regulating_AktGSK3b_Signaling_Pathway

[mgrade]

https://www.youtube.com/watch?v=AXF2gWuvhn0&app=desktop

[mgrade]

Pyridostigmine bromide  & Prostigmine Bromide implicated in Gulf War Syndrome

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2393741/

 

Pyridostigmine bromide & Prostigmine Bromide: Impairment of Long-Term Memory Formation and Neuropathological Changes

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364893/

Edited June 25, 2017 by mgrade

[Fawkinchit]

Just want to bump this thread. Still trying to make progress. 

[Jay1]

Profile pic makes me laugh every time

[gill]

On 4/10/2017 at 9:43 PM, dasitmane said:

So excitotoxicity via glutamate could be the culprit. 

 

 

Glutamate also causes synapse plasticity.   Perhaps it's just odd brain cell connections in response to odd chemicals.  For instance, if you have over-connectivity in visual areas, this could decrease inhibition, leading to things like trails. 

I don't think there'd be any way to directly counteract these changes though.  Gave up a long time ago looking for some direct cure.

[Fawkinchit]

On 11/27/2017 at 2:52 AM, Jay1 said:

Profile pic makes me laugh every time

Lol thanks Jay. How have you been?

20 hours ago, gill said:

Glutamate also causes synapse plasticity.   Perhaps it's just odd brain cell connections in response to odd chemicals.  For instance, if you have over-connectivity in visual areas, this could decrease inhibition, leading to things like trails. 

I don't think there'd be any way to directly counteract these changes though.  Gave up a long time ago looking for some direct cure.

Synapse plasticity most likely wouldn't be the case here, its a temporary condition and easily rectifiable.

Im still leaning towards neuronal loss, be it whatever the route, and likened to that in lithium overdose. 

[Fawkinchit]

A Recent Discovery

MDMA and MDA cause neurons to release a neurotransmitter called serotonin. Serotonin is important to many types of nerve cells, including cells that receive sensory information and cells that control sleeping and emotions. The released serotonin can over activate serotonin receptors. In animals, MDMA and MDA have been shown to damage and destroy nerve fibers of neurons that contain serotonin. This can be a big problem, because serotonin neurons have a role in so many things, such as mood, sleep, and control of heart rate.

Scientists have recently found that the damaged serotonin neurons can regrow their fibers, but the fibers don't grow back normally. The fibers may regrow into brain areas where they don't normally grow, but not into other brain areas where they should be located. The new growth patterns may cause changes in mood, learning, or memory.

[Fawkinchit]

The neurotoxicity of hallucinogenic amphetamines in primary cultures of hippocampal neurons.

Capela JP¹, da Costa Araújo S, Costa VM, Ruscher K, Fernandes E, Bastos Mde L, Dirnagl U, Meisel A, Carvalho F.

Author information

 

Abstract

3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") and 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) are hallucinogenic amphetamines with addictive properties. The hippocampus is involved in learning and memory and seems particularly vulnerable to amphetamine's neurotoxicity. We evaluated the neurotoxicity of DOI and MDMA in primary neuronal cultures of hippocampus obtained from Wistar rat embryos (E-17 to E-19). Mature neurons after 10 days in culture were exposed for 24 or 48 h either to MDMA (100-800 μM) or DOI (10-100 μM). Both the lactate dehydrogenase (LDH) release and the tetrazolium-based (MTT) assays revealed a concentration- and time-dependent neuronal death and mitochondrial dysfunction after exposure to both drugs. Both drugs promoted a significant increase in caspase-8 and caspase-3 activities. At concentrations that produced similar levels of neuronal death, DOI promoted a higher increase in the activity of both caspases than MDMA. In the mitochondrial fraction of neurons exposed 24h to DOI or MDMA, we found a significant increase in the 67 kDa band of apoptosis inducing factor (AIF) by Western blot. Moreover, 24h exposure to DOI promoted an increase in cytochrome c in the cytoplasmatic fraction of neurons. Pre-treatment with an antibody raised against the 5-HT(2A)-receptor (an irreversible antagonist) greatly attenuated neuronal death promoted by 48 h exposure to DOI or MDMA. In conclusion, hallucinogenic amphetamines promoted programmed neuronal death involving both the mitochondria machinery and the extrinsic cell death key regulators. Death was dependent, at least in part, on the stimulation of the 5-HT(2A)-receptors.

 

 

This basically proves that apoptosis from hallucinogenic overdose is a key factor. 

Edited November 28, 2017 by dasitmane

[Fawkinchit]

More evidence for glutamate related overexcitoxicity.

[Jay1]

On 28/11/2017 at 5:21 PM, dasitmane said:

Lol thanks Jay. How have you been?

Same old, same old really.... But hppd aside, life is ok... Riding the bitcoin rocket to the moon and have a nice job in the VR industry (when the tech advances, I have some interesting ideas on potentially helping hppd in VR)

Hope you are well

[Abdulvagap]

well with a lot more fruitful solution will come forth. medical procedures usually take a lot of research,time and effort. rcparmachemsolutions

[bpl4269]

I think the pathology of HPPD is too case sensitive and complex to be cured with a "magic bullet" 5HT2-a receptor antagonist. I understand why you might believe this to be an option, but in my experience, approaching treatment with narrow vision, so to speak, (no pun intended), is doomed to fail. Most of the substances that have landed many of us in this predicament have complex pharmacological profiles, some of which, either are incomplete, or we are unaware that they are incomplete. There is still much to be learned. Looking at the situation with a broader perspective enveloping every single receptor system affected, and possible/existing downstream effects of each individual drug, compiling that data, cross-referencing symptoms, drawing corresponding similarities, and creating a possible causative profile for each individual drug should be the goal. Though I have another theory, albeit, also case sensitive, but I believe it to possibly be applicable to the situations of some other individuals. Quick summation - Infectious disease, undiscovered or otherwise (lyme disease, bartonella, babesiosis, etc...) may be an induction precursor/catalyst to HPPD. The idea being that the brain's neurochemistry and the body's CNS is already weakened/unstable, and the ingestion of a drug, (especially neurotoxic RC's), can further the damage done to the brain/CNS by the illness, causing further and much more significant chaos to ensue. The reason I have so much invested in this particular theory is because I personally suffer from Lyme disease/bartonella, and it became abundantly clear to me that my HPPD would have never occurred had I been disease-free. I don't feel like going into too much more detail, but suffice to say, treating those diseases vastly improved my HPPD, and I'm certain that if I weren't such a late stage patient, and I wasn't ingesting cannabis, coffee and tobacco on a regular basis, my hppd would be entirely gone. I have come close to ridding it entirely in the past, but it has become less and less of a priority, as it is not nearly as severe as it used to be, and I have simply gotten used to it. Just my half baked thoughts. ha Take it as you will. 

[bpl4269]

Haven't been on this website or logged into this profile in years. I feel at home though. ha

[Fawkinchit]

https://www.ncbi.nlm.nih.gov/pubmed/22983118

more proof that hallucinogens cause neuronal excitotoxic apoptosis. Also note at the end that when the receptors are blocked it aids in the prevention and even halting of apoptosis. So antagonists should be a treatment in emergency cases of hallucinogen treatment, in ERs that is.

 

The neurotoxicity of hallucinogenic amphetamines in primary cultures of hippocampal neurons.

Capela JP1, da Costa Araújo S, Costa VM, Ruscher K, Fernandes E, Bastos Mde L, Dirnagl U, Meisel A, Carvalho F.

Author information

 

Abstract

3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") and 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) are hallucinogenic amphetamines with addictive properties. The hippocampus is involved in learning and memory and seems particularly vulnerable to amphetamine's neurotoxicity. We evaluated the neurotoxicity of DOI and MDMA in primary neuronal cultures of hippocampus obtained from Wistar rat embryos (E-17 to E-19). Mature neurons after 10 days in culture were exposed for 24 or 48 h either to MDMA (100-800 μM) or DOI (10-100 μM). Both the lactate dehydrogenase (LDH) release and the tetrazolium-based (MTT) assays revealed a concentration- and time-dependent neuronal death and mitochondrial dysfunction after exposure to both drugs. Both drugs promoted a significant increase in caspase-8 and caspase-3 activities. At concentrations that produced similar levels of neuronal death, DOI promoted a higher increase in the activity of both caspases than MDMA. In the mitochondrial fraction of neurons exposed 24h to DOI or MDMA, we found a significant increase in the 67 kDa band of apoptosis inducing factor (AIF) by Western blot. Moreover, 24h exposure to DOI promoted an increase in cytochrome c in the cytoplasmatic fraction of neurons. Pre-treatment with an antibody raised against the 5-HT(2A)-receptor (an irreversible antagonist) greatly attenuated neuronal death promoted by 48 h exposure to DOI or MDMA. In conclusion, hallucinogenic amphetamines promoted programmed neuronal death involving both the mitochondria machinery and the extrinsic cell death key regulators. Death was dependent, at least in part, on the stimulation of the 5-HT(2A)-receptors.

Edited February 12, 2018 by dasitmane

[Guest]

Yeah, but in order to have excitotoxicity the MDMA user has to overheat.