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Thread: Marijuana may prevent the onset of Alzheimer’s

  1. #1
    Distinguished Community Member Sherman Peabody's Avatar
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    Default Marijuana may prevent the onset of Alzheimer’s

    by Steve Elliott

    Early use of marijuana apparently delays — and might even prevent — the onset of Alzheimer’s disease, according to a leading scientist in the field. But the work of longtime researcher Gary Wenk of Ohio State University has come to a halt, despite the promising results.

    “We found out that people who smoked dope in the 1960s were not getting Alzheimer’s,” Wenk explained, reports KJ Hiramoto at the Seattle PI. “These 90-year-olds without dementia were telling us things like, ‘Well, I drank whiskey and smoked dope,’ and these are the things they remember. They don’t remember habits like how often they ate broccoli.”

    Maddeningly, Wenk’s research ground to a halt due to political, legal and financial reasons.

    “The evidence in animals is clear but making the leap to humans means that you have to find a drug company willing to handle the lawsuits and the money,” Wenk said.

    He faced other hurdles, as well. Scientists who wish to research marijuana have to compete for approval and grants from the National Institute on Drug Abuse (NIDA), for which The University of Mississippi is the only source of marijuana. You see, Ole Miss has the only federally legal, grant-funded cannabis garden in the U.S.A.

    What makes the situation even worse is that, as admitted even by NIDA Director Nora D. Valkow, M.D., is that the agency is only interested in studying the potential harms of marijuana — not the medicinal benefits.

    A spokesperson for the NIDA told the New York Times in 2010 that the agency “does not fund research focused on the potential medical benefits of marijuana.”

    “As the National Institute on Drug Abuse, our focus is primarily on the negative consequences of marijuana use,” NIDA spokeswoman Shirley Simson told the Times.

    And under federal law, the NIDA must approve all clinical research involving cannabis. It tightly controls which investigators are allowed access to the federal government’s Ole Miss marijuana supply, which is grown (and then stored, for years) at the research facility in Oxford, Mississippi.

    Catch-22, anyone?

    “I am not funded to do marijuana research,” Wenk said. “It cost me about $100,000 to do a whole experiment, $10,000 just to buy the molecule, and every old rat is $150. You can see how things add up, and individuals can’t afford them.”

    British researchers find corroborating evidence

    A paper published in the British Journal of Pharmacology suggests that the cannabinoids in marijuana are likely not only to prevent the onset of Alzheimer’s, but also of Parkinson’s disease, Huntington’s disease, and age-related dementia, reports Brandon Isaak at the Marijuana Policy Project.

    Chronic brain inflammation, oxidative stress, and intra-cellular dysfunction are the primary reasons people develop these debilitating neurological diseases, and the study found that both THC and CBD, found in marijuana, help protect nerve cell function in users, significant reducing these harmful conditions.

    The cannabinoids tap into the endocannabinoid system, reducing inflammation, protecting brain cells from oxidative damage, and promoting cellular health on multiple levels, according to the researchers.

    Showing promise: ‘Old people are going to win’

    Wenk’s research — before it was halted, anyway — was showing promise to middle-aged and older Americans. Cannabinoids found in marijuana may delay the onset of Alzheimer’s so effectively that people are more likely to die of old age before showing any signs of dementia.

    In the study, Wenk dosed rats in his lab at Ohio State a dosage equivalent to one puff of marijuana every day. In old rats that had impaired memory due to brain inflammation, that single puff a day was making them smarter. Not only were they more intelligent, but some of the pathological changes in the rats’ brains — due to aging — were being reversed.

    “Essentially, what we found was that we know that as people get older, their neurogenesis drops to zero,” Wenk said, referring to the process through which new brain cells are created. “And that’s part of the reason old people have a problem with their memory and depression. What we found was that not only did the single puff a day reverse the memory impairment but also restarted neurogenesis.”

    According to Wenk, delaying the end of neurogenesis (which means the regeneration of neurons) helps middle-aged Americans and their families in a very easy-to-measure way: in their pocketbooks.

    “If we can keep a person out of a nursing home for five years, we’ve saved that family and their insurance companies an awful lot of money,” Wenk said. “No matter how we spin this, old people are going to win.”

    “I’m incredibly excited about it, because this is the first time we’ve ever had a compound that actually works in the old brain,” Wenk said. “Everything works in the young brain, but this is working in old brains. So this means if you’re, 60, 70, and you’re having problems with mental decline? We might have a mechanism that could target that.”

    "Very low doses are effective," Wenk said — even just one puff of marijuana a day helps, according to his research. "This is just the beginning of what we believe we’ll uncover as we investigate this line of research,” he said.

    Blocking endocannabinoids may trigger early Alzheimer’s

    Another study from a team of investigators at the Stanford University School of Medicine led by Daniel Madison has implicated the blocking of endocannabinoids — the brain’s own internal versions of the active compounds in cannabis — in the early pathology of Alzheimer’s.

    It seems a substance called A-beta, suspected to play a key role in Alzheimer’s because it’s the main part of clumps which dot the brains of Alzheimer’s patients, may, in the early stages of the disease, impair learning and memory by blocking the beneficial action of endocannabinoids.

    The group at Stanford is now trying to suss out the molecular details of how this occurs. Pinning down the details could pave the path to new ways to stave off the learning disabilities and memory deficits that characterize Alzheimer’s — and could also help explain how smoking marijuana helps to delay or even prevent its onset.

    In the study, published in the June 28, 2014 issue of the scientific journal Neuron, the researchers detail how pyramidal cells in the brain underpin learning and memory. This assures, they learned, that high-intensity input such as falling down or burning your finger tends to stick in your memory, thus presumably help avoid such mishaps in the future.

    Pyramidal cells are encouraged to ignore “noise” signals — they constantly receive random signals from upstream nerve cells — by a sort of “wet blanket” nerve cells called interneurons. These secret an inhibitory substance, the molecular equivalent of an indifferent shrug or yawn, signaling that the input is not really very important.

    But when the news actually is significant, pyramidal cells secrete their own “Now just you wait a minute, this is important!” chemicals. And guess what? Those chemicals which signal the importance of incoming information are none other than the endocannabinoids.

    Madison speculates that when we smoke marijuana, the phytocannabinoids from the plant have the effect of enhancing the perceived “importance” of events that happen while we’re under the influence of pot.

    And another likely effect is inhibiting the “wet blanket” effect of interneurons — which, in Alzheimer’s, needs reducing to increase the ability to learn and remember.

    Increasing tolerance

    The federal Schedule I illegality of marijuana, under which it is officially considered to have no medical uses and a high danger of abuse, has stymied Wenk’s research. But the scientist has noticed a refreshing trend — a major shift in the cultural tolerance of cannabis, particularly from young people, including his students.

    “I have really seen a shift in 10 years of increased marijuana tolerance,” Wenk said. “In my class, people are more than willing to discuss their marijuana use. But they would be embarrassed to mention that they smoke cigarettes.”

    With Alzheimer’s ranking as the sixth leading cause of death in the United States — and with more than five million Americans currently struggling with the disease, which has no known cure — you’d think that lab results as promising as Wenk’s would have attracted major funding by now. But that’s not the case, because, as we’ve pointed out, the NIDA isn’t really interested in knowing about the medical benefits of marijuana — just its dangers.

    Wenk, who has researched the effects of Alzheimer’s on animals for about 40 years, has shared his findings in his book, Your Brain On Food.

    https://tokesignals.com/marijuana-sh...ch-is-stalled/
    Last edited by Sherman Peabody; 11-25-2017 at 02:15 PM.

  2. #2

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    Quote Originally Posted by Sherman Peabody View Post
    This quote is hidden because you are ignoring this member. Show Quote
    by Steve Elliott

    Early use of marijuana apparently delays — and might even prevent — the onset of Alzheimer’s disease, according to a leading scientist in the field. But the work of longtime researcher Gary Wenk of Ohio State University has come to a halt, despite the promising results.

    “We found out that people who smoked dope in the 1960s were not getting Alzheimer’s,” Wenk explained, reports KJ Hiramoto at the Seattle PI. “These 90-year-olds without dementia were telling us things like, ‘Well, I drank whiskey and smoked dope,’ and these are the things they remember. They don’t remember habits like how often they ate broccoli.”

    Maddeningly, Wenk’s research ground to a halt due to political, legal and financial reasons.

    “The evidence in animals is clear but making the leap to humans means that you have to find a drug company willing to handle the lawsuits and the money,” Wenk said.

    He faced other hurdles, as well. Scientists who wish to research marijuana have to compete for approval and grants from the National Institute on Drug Abuse (NIDA), for which The University of Mississippi is the only source of marijuana. You see, Ole Miss has the only federally legal, grant-funded cannabis garden in the U.S.A.

    What makes the situation even worse is that, as admitted even by NIDA Director Nora D. Valkow, M.D., is that the agency is only interested in studying the potential harms of marijuana — not the medicinal benefits.

    A spokesperson for the NIDA told the New York Times in 2010 that the agency “does not fund research focused on the potential medical benefits of marijuana.”

    “As the National Institute on Drug Abuse, our focus is primarily on the negative consequences of marijuana use,” NIDA spokeswoman Shirley Simson told the Times.

    And under federal law, the NIDA must approve all clinical research involving cannabis. It tightly controls which investigators are allowed access to the federal government’s Ole Miss marijuana supply, which is grown (and then stored, for years) at the research facility in Oxford, Mississippi.

    Catch-22, anyone?

    “I am not funded to do marijuana research,” Wenk said. “It cost me about $100,000 to do a whole experiment, $10,000 just to buy the molecule, and every old rat is $150. You can see how things add up, and individuals can’t afford them.”

    British researchers find corroborating evidence

    A paper published in the British Journal of Pharmacology suggests that the cannabinoids in marijuana are likely not only to prevent the onset of Alzheimer’s, but also of Parkinson’s disease, Huntington’s disease, and age-related dementia, reports Brandon Isaak at the Marijuana Policy Project.

    Chronic brain inflammation, oxidative stress, and intra-cellular dysfunction are the primary reasons people develop these debilitating neurological diseases, and the study found that both THC and CBD, found in marijuana, help protect nerve cell function in users, significant reducing these harmful conditions.

    The cannabinoids tap into the endocannabinoid system, reducing inflammation, protecting brain cells from oxidative damage, and promoting cellular health on multiple levels, according to the researchers.

    Showing promise: ‘Old people are going to win’

    Wenk’s research — before it was halted, anyway — was showing promise to middle-aged and older Americans. Cannabinoids found in marijuana may delay the onset of Alzheimer’s so effectively that people are more likely to die of old age before showing any signs of dementia.

    In the study, Wenk dosed rats in his lab at Ohio State a dosage equivalent to one puff of marijuana every day. In old rats that had impaired memory due to brain inflammation, that single puff a day was making them smarter. Not only were they more intelligent, but some of the pathological changes in the rats’ brains — due to aging — were being reversed.

    “Essentially, what we found was that we know that as people get older, their neurogenesis drops to zero,” Wenk said, referring to the process through which new brain cells are created. “And that’s part of the reason old people have a problem with their memory and depression. What we found was that not only did the single puff a day reverse the memory impairment but also restarted neurogenesis.”

    According to Wenk, delaying the end of neurogenesis (which means the regeneration of neurons) helps middle-aged Americans and their families in a very easy-to-measure way: in their pocketbooks.

    “If we can keep a person out of a nursing home for five years, we’ve saved that family and their insurance companies an awful lot of money,” Wenk said. “No matter how we spin this, old people are going to win.”

    “I’m incredibly excited about it, because this is the first time we’ve ever had a compound that actually works in the old brain,” Wenk said. “Everything works in the young brain, but this is working in old brains. So this means if you’re, 60, 70, and you’re having problems with mental decline? We might have a mechanism that could target that.”

    "Very low doses are effective," Wenk said — even just one puff of marijuana a day helps, according to his research. "This is just the beginning of what we believe we’ll uncover as we investigate this line of research,” he said.

    Blocking endocannabinoids may trigger early Alzheimer’s

    Another study from a team of investigators at the Stanford University School of Medicine led by Daniel Madison has implicated the blocking of endocannabinoids — the brain’s own internal versions of the active compounds in cannabis — in the early pathology of Alzheimer’s.

    It seems a substance called A-beta, suspected to play a key role in Alzheimer’s because it’s the main part of clumps which dot the brains of Alzheimer’s patients, may, in the early stages of the disease, impair learning and memory by blocking the beneficial action of endocannabinoids.

    The group at Stanford is now trying to suss out the molecular details of how this occurs. Pinning down the details could pave the path to new ways to stave off the learning disabilities and memory deficits that characterize Alzheimer’s — and could also help explain how smoking marijuana helps to delay or even prevent its onset.

    In the study, published in the June 28, 2014 issue of the scientific journal Neuron, the researchers detail how pyramidal cells in the brain underpin learning and memory. This assures, they learned, that high-intensity input such as falling down or burning your finger tends to stick in your memory, thus presumably help avoid such mishaps in the future.

    Pyramidal cells are encouraged to ignore “noise” signals — they constantly receive random signals from upstream nerve cells — by a sort of “wet blanket” nerve cells called interneurons. These secret an inhibitory substance, the molecular equivalent of an indifferent shrug or yawn, signaling that the input is not really very important.

    But when the news actually is significant, pyramidal cells secrete their own “Now just you wait a minute, this is important!” chemicals. And guess what? Those chemicals which signal the importance of incoming information are none other than the endocannabinoids.

    Madison speculates that when we smoke marijuana, the phytocannabinoids from the plant have the effect of enhancing the perceived “importance” of events that happen while we’re under the influence of pot.

    And another likely effect is inhibiting the “wet blanket” effect of interneurons — which, in Alzheimer’s, needs reducing to increase the ability to learn and remember.

    Increasing tolerance

    The federal Schedule I illegality of marijuana, under which it is officially considered to have no medical uses and a high danger of abuse, has stymied Wenk’s research. But the scientist has noticed a refreshing trend — a major shift in the cultural tolerance of cannabis, particularly from young people, including his students.

    “I have really seen a shift in 10 years of increased marijuana tolerance,” Wenk said. “In my class, people are more than willing to discuss their marijuana use. But they would be embarrassed to mention that they smoke cigarettes.”

    With Alzheimer’s ranking as the sixth leading cause of death in the United States — and with more than five million Americans currently struggling with the disease, which has no known cure — you’d think that lab results as promising as Wenk’s would have attracted major funding by now. But that’s not the case, because, as we’ve pointed out, the NIDA isn’t really interested in knowing about the medical benefits of marijuana — just its dangers.

    Wenk, who has researched the effects of Alzheimer’s on animals for about 40 years, has shared his findings in his book, Your Brain On Food.

    https://tokesignals.com/marijuana-sh...ch-is-stalled/
    Personally I can't agree to the view that marijuana or any other pot herbs can help when it comes to conditions like Alzheimer. Such herbs affect our health, not in a good way. but in a bad way.

    Just imagine, what will be out condition after taking few puffs of Marijuana? Few of my friends say it's heaven but I can't subscribe to their views. We think we are in heaven beuase we lose our ability to percieve things. And, when our brain is used to such "high" things, It is usal that it will damage the brain rather than helping it.

    It is just my personal view .

  3. #3

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    I have been reading quite a bit about using CDB oil to slow the progression of Alzheimer and found out that medical cannabis has been proved to be a lot more effective in halting the progression of this devastating disease in comparison to the drugs that are normally prescribed for the treatment of Alzheimer’s.

  4. #4
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    J Neurosci. 2007 Sep 5;27(36):9*537-44.

    Nonpsychoa*ctive cannabidio*l prevents prion accumulati*on and protects neurons against prion toxicity.

    Dirikoc S, Priola SA, Marella M, Zsürger N, Chabry J.

    Institut de Pharmacolo*gie Moléculair*e et Cellulaire*, Unité Mixte de Recherche 6097, Centre National de la Recherche Scientifiq*ue, 06560 Valbonne, France.

    Abstract

    Prion diseases are transmissible neurodegenerative disorders characterized by the accumulation in the CNS of the protease-resistant prion protein (PrPres), a structurally misfolded isoform of its physiological counterpart PrPsen. Both neuropathogenesis and prion infectivity are related to PrPres formation. Here, we report that the nonpsychoactive cannabis constituent cannabidiol (CBD) inhibited PrPres accumulation in both mouse and sheep scrapie-infected cells, whereas other structurally related cannabinoid analogs were either weak inhibitors or noninhibitory. Moreover, after intraperitoneal infection with murine scrapie, peripheral injection of CBD limited cerebral accumulation of PrPres and significantly increased the survival time of infected mice. Mechanistically, CBD did not appear to inhibit PrPres accumulation via direct interactions with PrP, destabilization of PrPres aggregates, or alteration of the expression level or subcellular localization of PrPsen. However, CBD did inhibit the neurotoxic effects of PrPres and affected PrPres-induced microglial cell migration in a concentration-dependent manner. Our results suggest that CBD may protect neurons against the multiple molecular and cellular factors involved in the different steps of the neurodegenerative process, which takes place during prion infection. When combined with its ability to target the brain and its lack of toxic side effects, CBD may represent a promising new anti-prion drug.

    http://www.jneurosci.org/content/27/36/9537.abstract

    http://www.jneurosci.org/content/27/36/9537.full
    http://www.ncbi.nlm.nih.gov/pubmed/17804615

    THURSDAY, JUNE 30, 2016

    "Although other studies have offered evidence that cannabinoids might be neuroprotective against the symptoms of Alzheimer's, we believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells," says Salk Professor David Schubert, the senior author of the paper.

    Cannabinoids remove plaque-forming Alzheimer's proteins from brain cells

    https://www.eurekalert.org/pub_relea...-crp062816.php

    http://betaamyloidcjd.blogspot.com/2...e-forming.html

    National Cancer Institute at the National Institutes of Health

    Cannabis and Cannabinoids (PDQ®), Cancer Antitumor Effects, Prion prevention, Pain management, muscle relaxer, and Palliative Medicine

    Cannabis and Cannabinoids (PDQ®)

    Laboratory/Animal/Preclinical Studies

    Antitumor Effects Appetite Stimulation Analgesia

    Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis sativa and Cannabis indica species.[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.

    Antitumor Effects

    One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]

    Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis.[9-11] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[12]

    The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in hepatocellular carcinoma (HCC).[13] Both agents reduced the viability of hepatocellular carcinoma cells in vitro and demonstrated antitumor effects in hepatocellular carcinoma subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma[14] and breast cancer.[15]

    In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[16] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[17,18]

    In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[19] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[20-23]

    Appetite Stimulation Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[24] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[25]

    Analgesia Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[26] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[27,28]

    Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[29-31]

    References

    http://www.cancer.gov/cancertopics/p...essional/page4

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