Saturday, August 13, 2022

Does Acid Kill Brain Cells

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Viii Use Of Animal Models

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More important, however, has been the use of animal models to dissect the underlying neuropharmacology and physiology of psychedelics. During the past 5 decades, when human research was essentially nonexistent, numerous laboratories continued to study the effects of psychedelics in animal models. In vitro and ex vivo receptor binding studies, production of second messenger signals, use of receptor-specific antagonists, and even whole-animal imaging have given insight into the possible pharmacological and neurochemical effects of psychedelics. Indeed, many of those experiments would have been impossible to carry out in humans. The result has been a further and much more detailed understanding of the role that the 5-HT2A receptor, and other receptors, plays in normal brain function.

Overall, at least in rodent models, psychedelics seem to exacerbate neophobia, increase responsiveness to sensory stimulation, and interfere with response habituation across multiple sensory modalities and behavioral responses . A review of the use of animal models of serotonergic psychedelics was recently published .

Does Lsd Kill Brain Cells Debunking This Common Myth

No, theres no evidence that LSD kills brain cells whatsoever. However, it can have some long-lasting repercussions, both good and bad.

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  • One of the biggest misconceptions about LSD, and psychedelics in general, is that they kill your brain cells or damage the brain.

    While there are certainly some psychedelics that have been shown to cause harm most of the classical psychedelics have a surprisingly low potential for harm.

    LSD, in particular, has very a very low impact on the body and a profound impact on the mind . It attaches itself to various receptors in the brain to activate or deactivate certain regions but lacks any overt levels of toxicity that could lead to brain damage.

    Here, well explain in greater detail what LSD actually does to the brain and why you shouldnt be worried about brain damage if youve taken LSD in the past.

    Lsds Effects On The Serotonin Receptors

    The primary mechanism of action for LSD is its ability to bind to the serotonin receptors.

    Serotonin is one of the many different neurotransmitters throughout the body and is typically associated with pleasant and happy feelings and the changing of our mood and sleep.

    LSD binds itself to the principal serotonin receptors in the body, 5HT2A, and 5HT2C this interaction with these receptors causes serotonin to be released, heavily correlated with the feelings of joy and alterations in sensory perception after taking LSD .

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    Green Tea And Matcha Tea

    Green tea has many useful functions, including the ability to kill cancer stem cells. Scientists at Nanjing Medical University and Sun Yat-Sen University Cancer Center in China studied the effect of the green tea polyphenol, epigallocatechin-3-gallate , in the lab and found that it could reduce the growth of colon cancer stem cells by 50 percent.

    In addition, EGCG forced the cancer stem cells to commit cell suicide through the process of apoptosis. Another study from the University of Salford in England showed that matcha green tea, a form of powderized tea leaf, can interrupt the metabolic pathway of breast cancer stem cells, depriving them of energy and causing them to die. The effect of the EGCG in green tea on targeting cancer stem cells may help explain the protective effects of tea against colon and other cancers.

    Determination Of Paraoxonase Activity

    Can LSD Kill Brain Cells? How Acid Affects Your Brain

    Arylesterase activity of paraoxonase was measured spectrophotometrically in supernatants using phenyl acetate as a substrate.25,26 In this assay, arylesterase/paraoxonase catalyzes the cleavage of phenyl acetate resulting in phenol formation. The rate of formation of phenol is measured by monitoring the increase in absorbance at 270nm at 25°C. The working reagent consisted of 20mM Tris/HCl buffer containing 1mM calcium chloride and 4mM phenyl acetate as the substrate. Samples diluted 1:3 in buffer are added and the change in absorbance is recorded following a 20s lag time. Absorbance at 270nm was taken every 15s for 120s using a UV-Vis Recording Spectrophotometer . One unit of arylesterase activity is equal to 1 M of phenol formed per minute. The activity is expressed in kU/L, based on the extinction coefficient of phenol of 1310M/cm at 270nm, pH 8.0, and 25°C. Blank samples containing water are used to correct for the spontaneous hydrolysis of phenyl acetate.

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    How A Tangled Protein Kills Brain Cells Promotes Alzheimer’s

      Look deep inside the brain of someone with Alzheimers disease, most forms of dementia or the concussion-related syndrome known as chronic traumatic encephalopathy and youll find a common suspected culprit: stringy, hairball-like tangles of a protein called tau.

      Such conditions, collectively known as tauopathies strike scores of people across the globe, with Alzheimers alone affecting six million people in the United States.

      But more than a century after German psychiatrist Alois Alzheimer discovered tau tangles, scientists still have much to learn about them.

      A University of Colorado Boulder study, published this week in the journal Neuron, shows for the first time that tau aggregates gobble up RNA, or ribonucleic acid, inside cells and interfere with an integral mechanism called splicing, by which cells ultimately produce needed proteins.

      Understanding how tau leads to neurodegeneration is the crux of not just understanding Alzheimers disease but also multiple other neurological diseases, said senior author Roy Parker, a professor of biochemistry and director of the BioFrontiers Institute at CU Boulder. If we can understand what it does and how it goes bad in disease we can develop new therapies for conditions that now are largely untreatable.

      For part of his medical training, Lester worked alongside doctors and patients at the CU Alzheimers and Cognition Center in Aurora, seeing up close how critically more research is needed.

      Evan Lester

      Top 5 Cancer Stem Cell

      By William W. Li, MD

      Finding ways to kill cancer stem cells has been one of the holy grails in cancer research. While this is a target of biotechnology companies working on cancer treatment, scientists have already discovered dietary factors that have the ability to kill cancer stem cells, at least in some forms of cancer.

      Cancer stem cells are responsible for initiating many cancers, as well as igniting the recurrence of cancers after treatment. Here are the top cancer stem cell-killing foods

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      Psychological Or Psychiatric Issues

      Individuals who chronically abuse methamphetamine are more susceptible to the development of severe psychiatric disorders, including issues with psychotic-like behaviors, such as delusions, hallucinations, impaired reality testing, etc. Some of these psychotic-like behaviors can be rather idiosyncratic. For example, the term meth bugs refers to a psychiatric condition where chronic methamphetamine users have a sensation that their skin is crawling or itching with bugs even though no external stimulation is occurring. This condition will often remit but may return spontaneously in some individuals.

      Individuals who enter a formal substance use disorder treatment program and are successful in maintaining abstinence often recover some level of functioning however, in many cases, significant residual effects remain. Research indicates that there is quite a bit of variability in recovery that is often related to a number of personal variables as well as the length and seriousness of an individualâs use of methamphetamine.

      B Possible Use In Depression

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      The first report describing use of LSD in treating depression was in 1952 . There were no controls, and LSD was given in variable daily doses for 1 month. Savage concluded that improvement obtained using LSD therapy was no better than therapy without LSD but did state that therapeutically valuable insights into unconscious processes were gained. Since then, virtually nothing has been reported to suggest that psychedelics might have specific efficacy against endogenous depression. Nonetheless, studies cited in the previous section concerning treatment of anxiety and depression secondary to a cancer diagnosis do indicate that psychedelics may be effective in treating depression. A small, open-label study of ayahuasca in relieving depression reported by Osorio et al. is also suggestive. It remains to be proven whether psychedelics can be useful for treating MDD.

      There is good reason to believe that psychedelics might have efficacy in treating depression, however. For example, it has been shown that cortical 5-HT2A receptor expression is increased in postmortem samples of depressed and suicidal patients , whereas 5-HT2A binding was decreased in the hippocampus of depressed patients . Furthermore, it has been shown that medication-free depressed patients with high pessimistic attitudes have increased 5-HT2A receptor binding in the PFC compared with healthy control subjects .

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      Psychedelic Drugs May Change The Structure Of Brain Cells

      ByYasemin Saplakoglupublished 13 June 18

      It’s no surprise that psychedelic drugs such as LSD and ecstasy alter brain function, leading to the drugs’ “trippy” effects and possible hallucinations. But now, researchers have shown that these drugs can also physically alter the brain, changing the structure of brain cells.

      The new study was done on nerve cells in lab dishes and in animals, but if the findings also hold true in humans, these drugs could have surprising benefits for patients with certain mood disorders, the researchers said.

      That’s because, in people with depression or mood and anxiety disorders, neurons in the prefrontal cortex an area of the brain that’s important in part for controlling emotion tend to shrivel up, said senior study author David Olson, an assistant professor of chemistry, biochemistry and molecular medicine at the University of California, Davis. What’s more, the branches and dendritic spines on the neurons’ branches which they use to communicate with other neurons tend to retract, he said.

      In the study, published today in the journal Cell Reports, Olson and his team found that psychodelic drugs increase the number of branches and dendritic spines on neurons, and also increase the number of synapses, or connections between neurons.

      In the next part of the study, the researchers gave psychedelics to fruit flies and found that the number of branches in their neurons again increased with the drugs.

      C Psychedelics Can Engender Ecstatic States With Persistent Positive Personality Change

      The experimental study of mystical or ecstatic states engendered by psychedelics perhaps began with the so-called Good Friday experiment, carried out at Boston Universitys Marsh Chapel in 1962 by Walter Pahnke as his research for the Ph.D. in religion and society at the Harvard Divinity School. Pahnke examined the similarities and differences between experiences described by mystics and those induced by psilocybin. On Good Friday in 1962, 20 Christian theological student volunteers attended a 2.5-hour religious service in Boston Universitys Marsh Chapel. The setting and preparation of the subjects was designed to optimize a spiritual or mystical experience. In a double-blind procedure, subjects were given either an oral dose of 30 mg psilocybin, or a 200-mg placebo dose of nicotinic acid, administered in identical capsules. Based on responses to a variety of instruments and questionnaires, subjects who received psilocybin had experiences that were indistinguishable from those experienced by mystics. The experiences were powerful and personally meaningful. Doblin reported a follow-up to the Pahnke study in 1989 and was able to locate and interview 19 of the original 20 experimental participants. All of the psilocybin subjects felt that the experience had significantly affected their lives in a positive way and they expressed appreciation for having participated in the experiment.

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      Ix Potential Therapeutic Value For Psychedelics

      Clinical research with psychedelics essentially ended with the passage of the Controlled Substances Act of 1970. As pointed out in the Introduction, there were more than a thousand clinical articles discussing 40,000 patients, several dozen books, and six international conferences on psychedelic drug therapy . There were serious attempts to employ LSD in various kinds of therapy, with major emphasis on treatment of alcoholism and other addictions , as well as issues related to death and dying . Other studies examined the use of psychedelics to treat anxiety and depression, schizophrenia, and even autism . A review of psychedelic-assisted therapy was recently published .

      After a long hiatus in clinical research, one of the most exciting and encouraging recent developments in this field has been the reintroduction of human treatment studies with psychedelics. Studies discussed in this section will be seen by the reader to reinforce the early belief that psychedelics might represent an important new treatment modality for a variety of disorders. The fact that these new and positive clinical findings had to be postponed for several decades dramatically illustrates the destructive capacity of politics to hinder potentially significant medical advances.

      Psychedelic Drug Triggers Growth Of New Brain Cells In Mice

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      Research in mice has found that N,N-dimethyltryptamine , one of the active ingredients of the psychedelic tea ayahuasca, can spark the creation of new nerve cells and improve spatial learning and performance in memory tasks.

      The scientists behind the new study speculate that the drug could serve to treat neurodegenerative disorders, such as Alzheimers disease and Parkinsons disease.

      Neurodegenerative diseases involve the progressive loss of nerve cells in affected parts of the brain or, in some cases, in other locations of the nervous system. One way to reverse the damage might be to restore the capacity to produce new nerve cells, which is known as neurogenesis.

      The generation of most nerve cells in the human body takes place before birth. However, some studies suggest that the creation of new neurons is possible in adulthood, though other researchers have disputed the findings.

      Ayahuasca, a tea that shamans in several South American countries use for ritual and healing purposes, is emerging as a surprising potential source of drugs that could stimulate neurogenesis.

      Preliminary studies have shown that the psychedelic brew has antidepressant properties. Its newly reported potential ability to promote the growth of new nerves in the brain may partly explain these effects.

      They have now discovered that DMT also stimulates neurogenesis in mice. In addition, it improves their performance in tests of spatial learning and memory.

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      F Possible Role Of Other Receptors

      Ray reported on receptor screening of 25 hallucinogens and analogs by the National Institute of Mental Health Psychoactive Drug Screening Program, with affinities of 10 additional drugs taken from the literature. The 35 drugs of the study had very diverse patterns of interaction, which may underlie some of the qualitative psychopharmacological differences between the drugs. Functional effects of the various compounds were not studied, however, which would have strengthened the conclusions and given more detailed insight into the possible relevance of receptors where some of the tested drugs had relatively high affinity.

      The evidence for involvement of 5-HT1A receptors in the behavioral actions of psychedelics has been gleaned primarily from animal studies. Halberstadt and Geyer reviewed the evidence and concluded that the 5-HT1A receptor can play an important role in the behavioral effects of tryptamine-type psychedelics. Several examples illustrating the importance of 5-HT1A receptor activation in the action of tryptamine hallucinogens are provided in the later sections of this review on animal models, but two examples are provided now to illustrate how these conclusions were developed.

      Potential Way To Repair Brain Damage In Multiple Sclerosis

      Date:
      Oregon Health & Science University
      Summary:
      Blocking a certain enzyme in the brain can help repair the brain damage associated with multiple sclerosis and a range of other neurological disorders.

      Researchers at Oregon Health & Science University have discovered that blocking a certain enzyme in the brain can help repair the brain damage associated with multiple sclerosis and a range of other neurological disorders.

      The discovery could have major implications for multiple sclerosis, complications from premature birth and other disorders and diseases caused by demyelination — a process where the insulation-like sheath surrounding nerve cells in the brain becomes damaged or destroyed. Demyelination disrupts the ability of nerve cells to communicate with each other, and produces a range of motor, sensory and cognitive problems in MS and other disorders.

      The study was published this week in the online edition of the Annals of Neurology. The study was conducted by a team of researchers led by Larry Sherman, Ph.D., who is a professor of cell and development biology at OHSU and a senior scientist in the Division of Neuroscience at the Oregon National Primate Research Center.

      The new study shows that the hyaluronic acid itself does not prevent the differentiation of myelin-forming cells. Rather, breakdown products generated by a specific enzyme that chews up hyaluronic acid — called a hyaluronidase — contribute to the remyelination failure.

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      Q Ive Heard That People With Fewer Years Of Formal Education Are At Higher Risk For Getting Alzheimers Am I Less Likely To Get It Because I Have An Advanced Degree

      According to Rosebud Roberts, M.B.Ch.B., a Mayo Clinic epidemiologist, and lead investigator in a study correlating age and lack of education with the risk of developing Alzheimers disease, People with more years of education may experience a loss of cognitive ability, but they can compensate better and thus they dont demonstrate the symptoms of mild cognitive impairment. Its as though their education protects them from exhibiting the effects of mild cognitive impairment.

      In the study, the prevalence of mild cognitive impairment also varied according to years of education, ranging from:

      • 25 percent in those with up to eight years of education,
      • 14 percent in those with nine to 12 years,
      • 9 percent in those with 13 to 16 years, and
      • 8.5 percent in those with greater than 16 years.53

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