dasitmane

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Everything posted by dasitmane

  1. The part of the brain that is effected is any area involving serotonin receptors. Which are very specific neurons that are compromised throughout the entire brain. The damage is very widespread. This research disregards neurogenesis, so the hippocampus is a mute point. Yes the axolotl brain is an animal brain, but is still compromised of the same cells, and similar architecture. The brain may do quite a bit, but it wont fully recover, even with neurogenesis. The study clearly shows that newly made neurons are incapable of reconnecting the long distance axonal growths that previously existed. Give those who recovered enough coffee and they will realize they haven't recovered. People adapt, people will even lie to themselves that they are fine to get on with their day, day after day. Their neuronal loss maybe wasn't nearly as bad as those who dont "recover". All cases recover to a degree, but massive brain trauma according to what im seeing here can only be repaired to a certain degree and by the laws of nature herself will never repair to 100% functionality. Not from what I can see. What you're saying is possible, that the brain can reconnect, is exactly what this study shows is not possible. The neurons that are newly generated simply just dont know to send their axons 2mm or more. The brain simply just wont reconnect like it was. Sorry. I did my best.
  2. Everything in our universe is quite simple, Push/pull concept, up down black white red blue north pole south pole day night sun black hole etc etc etc... well with our receptors its the same concept, agonist inverse agonist, I was thinking that maybe these very potent agonist of the 5ht2a receptors cause such an extreme push that things become out of balance, just like if you decreased suns gravity the earth would fall away, maybe we can utilize inverse 5ht2a agonists to accomplish the rebalancing of our receptors. unfortunately these dont exist that are on the market today, only in clinical trials, for the treatment of insomnia. Anyone have any ideas? Update: Full documentation of this disease can be found on page 24 post #478
  3. Today, I'm the bearer of bad news. This news was unforeseen, and is all in all, quite crushing. Looking through regenerative videos of salamanders today, I found and noticed that regeneration wasn't completely up to par. That even though the limb might regrow. It didn't grow back perfectly in most cases. Which had me wondering more about neuronal regeneration, and after just a little bit of reading, the reality of all of this has really, finally, and sadly, fallen in to place. Unless someone can prove me wrong. I'm actually so depressed about this, that Ill hardly elaborate like I usually do. But to put it plainly, the brain consists of neurons, and as most of you might know, neurons have axons, what I failed to realize in the beginning of this 6 year escapade, is that those axons in certain areas of the brain, are actually quite long. Take for example the picture of the brain that I have uploaded, the long strands are actually called axonal tracts, theyre long communicative groups of axons from neurons. When the neurons die, the axon dies. Heres where we lose. When these neurons are replaced with new neurons, the new neurons, do not and can not connect to the same long distance axonal path that was originally there. Rather, the newly generated neurons are primarily bound to attach its axons to the surrounding neurons. Thus not completely repairing the original function of the brain, even if humans could regenerate neurons. This proof can be seen in this article of the axolotl salamander, in the link posted. Also, dont be confused by the title, neuronal diversity is the main topic of the article, but they elaborate on these long distance axonal tracts not being able to reconnect due to the distance. Its a lot like even if humans could regenerate limbs, if you severed a ligament it would detach from the bone, and even though it could regenerate, or have the ability, it does not have the ability to reach out and reattach itself to the site it was originally attached to. This has to be performed by a surgeon. I do beg everyone to read this thoroughly to see if I have made any mistakes in my understanding. Granted I know that some recovery is possible. But its fairly evident our brains will never be the same. https://elifesciences.org/articles/13998 Adult axolotls can regenerate original neuronal diversity in response to brain injury Abstract The axolotl can regenerate multiple organs, including the brain. It remains, however, unclear whether neuronal diversity, intricate tissue architecture, and axonal connectivity can be regenerated; yet, this is critical for recovery of function and a central aim of cell replacement strategies in the mammalian central nervous system. Here, we demonstrate that, upon mechanical injury to the adult pallium, axolotls can regenerate several of the populations of neurons present before injury. Notably, regenerated neurons acquire functional electrophysiological traits and respond appropriately to afferent inputs. Despite the ability to regenerate specific, molecularly-defined neuronal subtypes, we also uncovered previously unappreciated limitations by showing that newborn neurons organize within altered tissue architecture and fail to re-establish the long-distance axonal tracts and circuit physiology present before injury. The data provide a direct demonstration that diverse, electrophysiologically functional neurons can be regenerated in axolotls, but challenge prior assumptions of functional brain repair in regenerative species. https://doi.org/10.7554/eLife.13998.001 “Open annotations (there are currently 0annotations on this page). eLife digest Humans and other mammals have a very limited ability to regenerate new neurons in the brain to replace those that have been injured or damaged. In striking contrast, some animals like fish and salamanders are capable of filling in injured brain regions with new neurons. This is a complex task, as the brain is composed of many different types of neurons that are connected to each other in a highly organized manner across both short and long distances. The extent to which even the most regenerative species can build new brain regions was not known. Understanding any limitations will help to set realistic expectations for the success of potential treatments that aim to replace neurons in mammals. Amamoto et al. found that the brain of the axolotl, a species of salamander, could selectively regenerate the specific types of neurons that were damaged. This finding suggests that the brain is able to somehow sense which types of neurons are injured. The new neurons were able to mature into functional neurons, but they were limited in their ability to reconnect to their original, distant target neurons. More research is now needed to investigate how the axolotl brain recognizes which types of neurons have been damaged. It will also be important to understand which cells respond to the injury to give rise to the new neurons that fill the injury site, and to uncover the molecules that are important for governing this regenerative process. https://doi.org/10.7554/eLife.13998.002 Introduction Under physiological conditions, the neurogenic capacity of the adult mammalian brain is largely restricted to two neurogenic niches, the subventricular zone of the lateral ventricle, which gives rise to interneurons of the olfactory bulb and the subgranular zone of the dentate gyrus, which generates granule cells of the hippocampus (Ming and Song, 2011). Neurons in other brain regions are only generated during embryonic development and are not replaced postnatally. In contrast to mammals, other vertebrates are endowed with superior capacity to regenerate multiple organs, including parts of the central nervous system (CNS). Among these, urodele amphibians like the axolotl (Ambystoma mexicanum) are endowed with the capacity to add new neurons to the brain throughout life (Maden et al., 2013) and can regenerate the spinal cord and parts of the brain after mechanical injury (Burr, 1916; Kirsche and Kirsche, 1964a; Butler and Ward, 1967; Piatt, 1955). Resection of the middle one-third of one hemisphere, but not the whole hemisphere, in the axolotl telencephalon results in reconstruction of the injured hemisphere to a similar length as the contralateral, uninjured side (Kirsche and Kirsche, 1964a; Kirsche and Kirsche, 1964b; Winkelmann and Winkelmann, 1970). Similarly, after mechanical excision of the newt optic tectum, new tissue fills the space produced by injury (Okamoto et al., 2007). Interestingly, in the newt, selective chemical ablation of dopaminergic neurons within a largely intact midbrain triggers regeneration of the ablated pool of neurons (Berg et al., 2010; Parish et al., 2007). In addition to urodeles, teleost fish have also been extensively studied for their capacity to regenerate the CNS and have led to the identification of some of the molecular signals involved in the regenerative process (Kizil et al., 2012). These studies highlight the value of regenerative organisms as models to understand the mechanisms that govern brain regeneration for possible application to the mammalian brain. However, the mammalian CNS is notoriously complex, and its ability to compute high-level functions, like those of the mammalian cerebral cortex, relies on the presence of a great diversity of neuronal subtypes integrated in specific long-distance and local circuits and working within a defined tissue architecture. Disruption of brain structure, connectivity, and neuronal composition is often associated with behavioral deficits, as observed in models of neurodevelopmental, neuropsychiatric, and neurodegenerative disease. It is therefore likely that functional regeneration of higher-order CNS structures will entail the regeneration of a great diversity of neuronal subtypes, the rebuilding of original connectivity, and the synaptic integration of newborn neurons in the pre-existing tissue. It is not known to what extent even regenerative species can accomplish these complex tasks, beyond their broad ability to generate new neurons and to rebuild gross brain morphology. It remains therefore debated whether any vertebrates are capable of true functional brain regeneration. Using the adult axolotl pallium as the model system, we have investigated whether a diverse array of neuronal subtypes can regenerate and whether their tissue-level organization, connectivity, and functional properties can also regenerate after mechanical injury. In contrast to the teleostean pallium, the everted nature of which makes linking distinct regions to their mammalian counterparts difficult (Northcutt, 2008), the gross neuroanatomy of the axolotl pallium, organized around two ventricles, shows clear similarities to that of the mammalian telencephalon. In addition, while the evolutionary origin of the mammalian cerebral cortex remains controversial (Molnár, 2011), it is likely that the axolotl pallium contains a basic representation of several of the neuronal subtypes found in the mammalian cerebral cortex and thus may serve as a good model for investigating regeneration of neuronal heterogeneity and complex circuit function. Here, we demonstrate that both pre- and post-metamorphosis adult axolotls are able to regenerate a diversity of neurons upon localized injury to the dorsal pallium. This process occurs through specific regenerative steps that we defined in live animals using non-invasive magnetic resonance imaging (MRI). Strikingly, newborn neurons can acquire mature electrophysiological properties and respond to local afferent inputs. However, they unexpectedly fail to rebuild long-distance circuit and the original tissue architecture. The data provide the first proof for the precision with which axolotls regenerate a diverse set of neurons, which in turn become electrophysiologically active and receive local afferent inputs. Notably, however, our results also challenge prior assumptions of functional brain regeneration in salamanders by uncovering unappreciated limitations in the capacity of adult axolotls to fully rebuild original long-distance connectivity and tissue organization, a finding that redefines expectations for brain regeneration in mammals.
  4. Thats weird, nicotine makes mine worse.
  5. Whatever you do dont do any hallucinogens again, even if the symptoms reside. You should see some recovery. The degree no one will know for sure. Give it about 6 months. It took a while but eventually my visual snow went away. Primarily now I just have really bad anxiety issues.
  6. Jesus man 48 years?? I dont think I even plan on sticking around if I cant find a cure for this.
  7. If you read my posts in the possibility of and idea for a cure thread, theres a great deal of answers and evidence of whats going on. The biggest problem is people just want to have fun and wont put time in to researching this.
  8. Yah, I'm not exactly sure either to be honest. But its clearly the link. I do wish this information was publicized instead of the ridiculous researchers investigating the "pros" of hallucinogens, if this information were available I never would have done them.
  9. No, the article clearly shows that the excitotoxity is a result from 5htp2a receptor activation. did you even read the study?
  10. 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.
  11. More evidence for glutamate related overexcitoxicity.
  12. 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.
  13. Sounds like you are a bit paranoid. Its not impossible, but it will take time to see if you have it. Based on what you are describing if you do have it its very mild. If youre paraplegia is caused by brain abnormalities rather than spinal it could make you more susceptible. Basically give it some time and see what happens. Basically though, DO NOT do hallucinogens again. They definitely do serious damage to the brain.
  14. 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.
  15. Lol thanks Jay. How have you been? 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.
  16. 6 years Edit: Man some people have had this a long time! I dont get the visual snow, dp/dr, or any visuals. I used to get the snow and dp/dr but they went away. Never had visuals. For me most of mine is manifested by a crippling anxiety, its almost unbearable, and just about anything can trigger it. As long as im not exposed to anything and dont drink too much coffee it typically ok. But to much coffee in the morning can make it bad. And some times it flares up and I dont have an explanation.
  17. Just want to bump this thread. Still trying to make progress.
  18. The cause of HPPD is fairly simple and very detailed in my ongoing thread. Its simply neuronal overexcitation leading to apoptosis. I've posted an endless amount of information showing its the only possible cause. Neurogenesis is the only possible cure for HPPD. Also the guys theory is easily disproved in the fact that if it were caused by immune dysfunction attacking the brain, it would most likely be a progressive disease. Which its not.
  19. 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
  20. Lol, based on the fact that he said "higher level of consciousness" I dont need to read the whole article to understand that he is an idiot. And who dictates what this forum is about? So who are you to say what its about? And as far as I'm concerned in all the research that I have done I'm easily ahead of the so called professionals in this disease, and based on your history you have made absolutely zero progress in the diagnosis nor treatment there of, so you have absolutely no room to speak. Edit: I actually read a little more of your most ridiculous statements and the fact that you think that psychedelics should be used on mentally ill/handicapped patients shows that you not only know absolutely nothing about neurology, but that you're a belligerent moron, a mere child running with scissors unrelentingly. Please put down the scissors, step away from your keyboard, and slap yourself repeating "I know not what I say" till you understand the reason for the therapy at hand. No pun intended, phaggot.
  21. Really!? The brain on hallucinogens acts different than normal!? HOLY FUKK what a way to waste a chit ton of tax money and time on a worthless research project. Loser fukk researcher should just retire now. What a worthless bitch. How stupid do you have to be to even publish those findings? "Brain doesn't act normal on psychedelics" hahaha nahhhhh I dont believe it. Professor Anil "Hurr Durr" Seth "higher 'level' of consciousness" Lol what a worthless piece of shit.
  22. In some of my free time I learned classical astrology and you can tell a lot about how a persons life will be. I would like to see if maybe some of us who got HPPD have anything in common astrologically. If you would like to contribute please post the exact time and location you were born. The time needs to be down to the minute, location is necessary as well. If you dont know the exact time it can be found on your birth certificate.
  23. 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 [
  24. 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.