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


Fawkinchit

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Note on 5HTP:

 

It is used to make serotonin.  You will see warning about taking it with MAOIs and SSRs for causing serotonin syndrome (too much serotonin).  Generally it is safe to take ... but that can be said of antibiotics, etc.  HPPDers get that way because some threshold of 'alteration' occurs.  Sometimes just a straw that breaks the camel's back.

 

Hope1, Have you ever tried SSRIs or tricyclics?

 

 

Note on Brain Damage:

 

Naturally, the very expression can scare people.  We don't, in contrast, get all worried about skinning our knee ... unless we are 3.

 

Because of aging, neurons die every day - hundreds or thousands even.  But even a very health person shows signs of brain aging ... little memory issues, shakiness, don't sleep as well, etc.  Resolving the fear of "brain damage" is the same as resolving the fear of eventually dying - it is philosophical and beyond the normal scope of posts in this forum.

 

Now, not everyone is so fortunate to have a wonderful, healthy, accident free life.  These regrettable factors increase the rate of neurons-go-bye-bye so cause a person to experience more problems as they age than they otherwise would have.  A dramatic example is getting a serious head injury in a car accident ... or having a stroke.

 

 

Note on Neurogenesis:

 

This occurs freely and readily in the body.  For example, a mild cut will sever many nerves, cause deaths, regenerations, and alteration.  And soon the finger feels just fine.  Occasionally a person will get a nasty cut and have some numbness or other change in sensation/perception.

 

In the brain, only a couple small areas have shown the ability to grow new neurons.  The rest does not.  One reason for this is that many neurons are quite long ... some have axons a meter long.  So people with spinal injuries, such as Christopher Reeves, suffer some significant problems that don't recover.  Another reason new neurons don't grow is because it usually isn't necessary.  Under good conditions, a neuron literally lasts a life time.  Changes (learning) occur via synaptic changes.  Synapsis are designed to readily form and change.  This design makes the brain very stable.  A new neuron is not stable until many connections (synapsis) are formed - on average, each neuron has ~1000 synaptic connections to it.

 

So in the end, we can be happy the way we are made.  And certainly there is little we can do to change this in a positive way.

 

 

Note on Excitotoxicity:

 

Neurons are Integrators, that is, adding machines that take in positive and negative integers.  These integers are ions that enter the cell via the synapsis.  When the sum reaches a certain level (an actual set negative voltage threshold), the electrical charge is neutralized by being discharged into the axon which causes chemical to be discharged out each synapsis.

 

All cells in the body are very complex chemical factories, churning out many different proteins, enzymes, and other molecules.  With each chemical (molecule) formed, there are waste products.  Many of these waste products are very chemically active and cause damage if they hang around and must be cleaned up by the cell.  Free radicals and reactive spieces are term you often hear that refer to this junk. 

 

As long as a cell can take care of the waste, it remains healthy.  What causes a cell to NOT care for wastes in a timely matter?  Several things can.  Insufficient cleanup materials (cellular malnutrition).  Genetic problems that omit or alter instruction on how to form some things.  Cellular activity too rapid to keep up.  Introduction of outside wastes or poisons.

 

The neuron has the added feature in that, it itself cannot control it's own firing rate (discharge down the axon).  Firing rate is entirely the sum of all the outside synaptic inputs.

 

The word Excitotoxicity is simple that the excitation rate (firing rate) is faster than the time required for the cell to clean up all the waste products.  The more this happens the more damage to the neuron.  If it stops in time and there is proper nutrition, the cell repairs and no harm done.  In the worse case scenario, the cell will literally fire itself to death - this can happen even in just a few minutes.

 

Do we have excitotoxicity issues?  With cerebral disinhibition there is too much activity.  Dr A used the term "pre-seizure".  And, note that the most effective meds are usually anti-seizure, namely Klonopin.

 

Anxiety is an example to too much neuron activity.  When autopsying a person who suffered chronic anxiety throughout their life, certain parts of the brain are ~12% smaller than their peers.  Smaller is always because cells died.

 

What can we do?  Limit stress - treat anxiety and depression.  Learn to chill out and enjoy life.  Eat well.  Drink clean water.  Breath clean air.  Limit alcohol and any other things that end up stressing the nervous system.  Eat foods and supplements that support the cellular clean-up-crews.

 

Is this easy?  No, but the more you do, the better the odds of good health.

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Was hoping drugs like NSI-189 or master gene regulator therapeutics would one day help. Settling or acceptance can work for some but not everybody. So this is it then? No hope of ever being cured in this lifetime?

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  • 2 weeks later...

If you go over everythimg that I have posted recently you can see that the excitotoxicity is from 5ht2a receptor activation,  its all in the notes, it goes 5ht2a agonist > 5ht2a receptor > glutamate release > excitotoxicity > neuronal apoptosis. Im sure its hard to take on and alot of people are going to just be in denial about cause brain damage seems like a dead end, but its not, neurogenesis is possible, and can be proven easily to be so, its just figuring out how.

 

Also damage to specific sites in the cerebellum is all Ive shown, im sure that there is damage to inhibitory cells also in the visual cortex, and there should be some in the lobes, 

 

Also didnt know that the cerebellum was involved with vision can you provide the information on that.

 

http://www.wayfinding.net/cerebell.htm

This wasn't the original article I derived that statement from.. Was a while back, and I can't seem to find it. But it is involved with vision.

I accept that there may be actual brain damage. Yet you didn't really address the other questions and statements I made..

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Maybe somebody ought to send the NIH a memo...

Institute/Center

National Institute of Neurological Disorders and Stroke (NINDS)

Contact

Christopher Thomas

301-496-5751

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Embargoed for Release: Wednesday, July 31, 2013, 8 a.m. EDT

NIH launches neurological drug development projects

New projects will target Fragile X syndrome, nicotine addiction, and age-related macular degeneration

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The National Institutes of Health has launched three innovative projects that will focus on development of therapeutics for Fragile X syndrome, nicotine addiction, and age-related macular degeneration (AMD). These projects are funded through the NIH Blueprint Neurotherapeutics Network which provides access to a variety of drug development resources.

“We are excited about the opportunity to apply cutting-edge science to the pursuit of novel treatments for these debilitating disorders” said Rebecca Farkas, Ph.D., program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS), Office of Translational Research.

The purpose of the NIH Blueprint is to provide in-depth research capabilities to increase the success rate of innovative drug discovery efforts. The program uses a virtual pharma model to provide researchers with access to support and resources that have been traditionally available to large pharmaceutical companies.

NIH Blueprint

Partnerships between NIH program staff and awarded research teams are designed to bridge the funding gap between ground-breaking laboratory research and industry adoption. NIH staff helps investigators work with veteran industry drug development consultants and contract research organization capabilities from the discovery stage through preliminary clinical trials. In addition, each investigator maintains sole ownership of intellectual property associated with his or her project

NIH launched the Blueprint Neurotherapeutics Network in 2011. Including these three awards, 14 drug discovery programs have been funded as part of the program and 10 are currently active (see: http://neuroscienceblueprint.nih.gov/bpdrugs/bpn.htm).

The newly-funded investigators and their organizations are:

Sage Therapeutics, Cambridge, Mass.

Principal Investigator: Al Robichaud, Ph.D.

Disorder: Fragile X syndrome

Project Summary: Fragile X syndrome is a genetic disorder linked to a range of neurodevelopmental disorders including learning disabilities and cognitive impairment. Many patients experience general and social anxiety yet benzodiazepines, which are drugs typically used to treat anxiety disorders, provide little relief. Their anxiety has been linked to reduced activity in the brain by a protein called, the GABA A receptor. Sage Therapeutics is developing positive allosteric modulators, designed to enhance the receptor’s activity and possibly relieve the anxiety.

The Scripps Research Institute, Jupiter, Fla.

Principal Investigator: Paul J. Kenny, Ph.D.

Disorder: nicotine addiction

Project Summary: Nicotine addiction has been attributed to the stimulatory effects of nicotine binding to brain proteins called orexin 1 receptors. Dr. Kenny and colleagues will develop selective receptor antagonists as potential smoking cessation aids to treat people who have attempted to quit smoking but faced high relapse rates and significant side effects.

University of Utah, Salt Lake City

Principal Investigator: Dean Yaw Li, Ph.D.

Disorder: age-related macular degeneration

Project Summary: Age-related macular degeneration is a leading cause of blindness in the United States. One form, called wet AMD, is associated with inflammation and blood vessel leakage in the retina, the eye’s light-sensitive tissue. Dean Li and his colleagues are developing small molecules that inhibit the activity of Arf6, a molecule known to help control inflammation and blood vessel leakage. This novel approach may lead to effective therapies for treating patients who do not respond to current wet AMD therapies.

NINDS is the nation’s leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease – a burden borne by every age group, by every segment of society, by people all over the world.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH...Turning Discovery Into Health®

###

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Wondering why they don't just try Stiripentol for Fragile X syndrome before developing a new positive allosteric modulator for GABAA receptors.

But yeah, if someone could produce the brainpower to be eloquent enough, then it would definitely be worth the try to drop a hint at the NIH.
Maybe David or Dr. Abraham could help in those regards (if they haven't already)? Though with protocol being as it is and all, I'd think the first necessary step would be to contact the DSM people.. But they just published version 5 I believe, so it might be a while before they update anything.

If only we could find some freelancing mad scientist to help us out here.

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So what's the story with corelactem?

I suggest you start reading here for general info, and here for updates. I'm considering to construct a document which comprehensively covers the theory behind why Coluracetam should work so well for HPPD, so I might post that later as well.

I saw you Aggressive Advocacy post.. It's a pity it didn't come off the ground. When I said "freelance mad scientist", I meant to refer more to "A competent scientist who doesn't care about protocol, finances, and law, yet still has a sense of ethics." Usually those are of the best kind.

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I'm just one guy.

Contact several thousand researchers by email and only received 2-3 responses. It's so shockingly upsetting that I have no words.

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Wow.. yeah I'm quite speechless about that myself. I might consider contacting Dutch researchers.. XTC is extremely popular here, and I'm sure the government would love a reason to rant on it (they've even been bitching about weed for years now..). Yet I rather do that without the scent of despair though.

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^Which is why one way to .. I just had an olfactory flashback of Iboga.. man that stuff tasted weird. Anyway, one way to get research going would be to give the government a reason to do so: it may support their "War on Drugs". Seriously, why couldn't they call it the "Endeavor for Sobriety"? Just shows how stupid they really are.

hope1: The only reason I haven't done so yet, is because I don't feel comfortable in my abilities to do so convincingly and eloquently. I presume I'd have a better chance at achieving scientific support once I'm in a better condition, as such I'm procrastinating that.

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You want to change transcription factors via talk therapy? Sure, environment has an impact on our genetic activation, but would you know what to say, how loud at what pitch etc. to turn on that gene that we need? Or am I totally getting the implication of this wrong?

 

asdf

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Hehe my bad, just gave it a quick zoom-zoom and thought "talk therapy - epigenetics - error".
I haven't gone through all your theories, but which gene transcription factor is it actually that you are looking to activate?
Lion's Mane activates ChAT transcription factors, if my reasoning is correct. Would seem to me to have potentially beneficial outcomes for HPPD, and up to now I can't think of any better-to-target genes than cholinomediating (yes I'm making up words) transcription factors.

Has anyone on this forum given Lion's Mane a fair chance? By fair I mean 2-5 grams a day of full-spectrum-all-parts-included LMM, for a minimum of 3 months? 'Cause that's one hell of an expensive venture if you don't buy bulk powder, as such doubtfully anyone has done so. Whoops sorry for derailing on LMM there, but it's quite relevant considering the genetic effects. Also, LMM is renown for its NGF stimulation, and I believe you said that neurogenesis is the key (or something similar, forgive my memory).

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