Tag Archives: neuroprotective

Researchers study neuroprotective properties in cannabis

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“With more states opting to legalize the sale of medical marijuana, researchers are taking a closer look at the use of cannabis to treat chronic illnesses.

Dr. Manny Alvarez, senior managing health editor of FoxNews.com, recently sat down with the Medicine Hunter, Chris Kilham, to find out how it’s being studied.

Dr. Manny: Now from the medical marijuana perspective, as far as the treatment of chronic illnesses, what is it about cannabis that makes it that special?

Medicine Hunter: Well, it seems that there are primarily two things – there’s the THC, that’s what people associated with getting high. And that appears to have a saliatory effect on the eyes in case of glaucoma. For people who are suffering from chemotherapy and can’t eat, it helps to get their appetite back. And we also know that it is a potent pain reliever – and science on that goes back to the 1890s.

But there’s another agent in cannabis that is getting more attention now, and that is called cannabidiol. And this is something that you can swallow by the bucket-full, and it won’t get you high at all. But it appears to have profound nerve-protective and brain-enhancing properties. And interestingly enough, it also induces an anti-anxiety effect.

So this appears to be a very important agent, perhaps useful in the treatment of neurodegenerative disorders.

DM: Are they extracting that particular chemical off the marijuana?

MH: There seem to be two pathways that people are taking.  You’ve got G.W. pharmaceuticals in Britain that has come out with a whole cannabis fluid spray. You’ve got people also isolating cannabidiol and playing with that in the lab.

I don’t know how this is all going to settle out – I mean, as a whole-plant person, I’m inclined toward the whole extract. But it does appear that this may also have anti-cancer properties, and that’s very intriguing.

DM: Is marijuana addictive?

MH: I would say that people can absolutely become dependent upon it.  But not physiologically addictive.  And, as you know, that’s not just parsing terms – I mean physiological addiction, you go through very grave withdrawal.

But people can become dependent on it just as they can on any substance.

DM: Tell me about this study in the American Journal of Pediatrics talking about pregnant Jamaican women and the use of pot.

MH: Melanie Dreher, who is the dean of nursing at Rush Medical Center inChicago, did a study in Jamaica. It was actually published in the American Journal of Pediatrics in 1994, but now it’s re-circulating because of all the interest in the neuroprotective properties.

Basically, she studied women during their entire pregnancy, and then studied the babies about a year after birth. And what she studied was a group of women who did smoke cannabis during pregnancy and those who didn’t. She expected to see a difference in the babies as far as birth weight and neuro tests, but there was no difference whatsoever. The differences that the researchers did notice, that are unexplained and kind of curious are that the babies of the women who had smoked cannabis — and we’re talking about daily use during their pregnancy — socialized more quickly, made eye contact more quickly and were easier to engage.

We don’t know why this is so, but all the old saws of smoking during pregnancy will result in low birth weight did not show up — at least in the Jamaican study. In U.S. studies where we’ve seen a similar investigation, women have concurrently been abusing alcohol and other drugs as well.

Alvarez said it’s interesting to note that there may be neuroprotective properties present in cannabis and the cannibidiol extract, but that smoking of any kind in pregnant women is discouraged.”

More research is needed when it comes to medical marijuana, he added.”

http://www.foxnews.com/health/2012/03/20/researchers-study-neuroprotective-properties-in-cannabis/

“Study: Cannabis may prevent brain damage” http://www.foxnews.com/health/2013/06/06/study-cannabis-may-prevent-brain-damage/

Cannabinoid as a neuroprotective strategy in perinatal hypoxic-ischemic injury.

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“Perinatal hypoxia-ischemia remains the single most important cause of brain injury in the newborn, leading to death or lifelong sequelae.

Because of the fact that there is still no specific treatment for perinatal brain lesions due to the complexity of neonatal hypoxic-ischemic pathophysiology, the search of new neuroprotective therapies is of great interest.

In this regard, therapeutic possibilities of the endocannabinoid system have grown lately.

The endocannabinoid system modulates a wide range of physiological processes in mammals and has demonstrated neuroprotective effects in different paradigms of acute brain injury, acting as a natural neuroprotectant.

Concerning perinatal asphyxia, the neuroprotective role of this endogenous system is emerging these years.

The present review mainly focused on the current knowledge of the cannabinoids as a new neuroprotective strategy against perinatal hypoxic-ischemic brain injury.

http://www.ncbi.nlm.nih.gov/pubmed/21788999

[The cannabinoid system and its importance in the perinatal period].

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“The cannabinoid system has been recently described, including the endogenous ligands, mainly arachidonic acid derivatives, and their specific receptors. Endocannabinoids are involved in the modulation of synaptic transmission, through which they exert their psychoactive, motor and antinociceptive effects, among others; they also exert extraneural effects, mainly immunomodulation and vasodilation.

Recent data suggest that the cannabinoid system might play an important role in human ontogeny and could participate in the implantation and early development of the embryo, in fetal brain development, and in the beginning of breast feeding after birth.

In addition, the vasodilatory effect of cannabinoids, together with inhibition of the release of excitotoxic amino acids and cytokines, as well as modulation of oxidative stress and the toxic production of nitric oxide, justify the growing evidence pointing to a possible neuroprotective effect of cannabinoids in perinatal asphyxia.”

http://www.ncbi.nlm.nih.gov/pubmed/16266619

Cannabinoids: well-suited candidates for the treatment of perinatal brain injury.

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“Perinatal brain injury can be induced by a number of different damaging events occurring during or shortly after birth… the number of clinical interventions available for the treatment of the affected newborn babies is extremely limited. Hence, there is a dramatic need to develop new effective therapies aimed to prevent acute brain damage and enhance the endogenous mechanisms of long-term brain repair.

The endocannabinoid system is an endogenous neuromodulatory system involved in the control of multiple central and peripheral functions. An early responder to neuronal injury, the endocannabinoid system has been described as an endogenous neuroprotective system that once activated can prevent glutamate excitotoxicity, intracellular calcium accumulation, activation of cell death pathways, microglia activation, neurovascular reactivity and infiltration of circulating leukocytes across the blood-brain barrier.

The modulation of the endocannabinoid system has proven to be an effective neuroprotective strategy to prevent and reduce neonatal brain injury in different animal models and species.

Also, the beneficial role of the endocannabinoid system on the control of the endogenous repairing responses (neurogenesis and white matter restoration) to neonatal brain injury has been described in independent studies.”

http://www.ncbi.nlm.nih.gov/pubmed/24961520

The Cannabinoid WIN55212-2 Promotes Neural Repair After Neonatal Hypoxia–Ischemia

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Figure 1.

“In the last years, cannabinoids have emerged as promising neuroprotective agents in several animal paradigms of acute and degenerative brain damage. Most neuroprotective effects of cannabinoids result from the activation of cannabinoid Type 1 (CB1R) and Type 2 (CB2R) receptors in neural and immune cells.

Besides, the stimulating effect of cannabinoids on proliferation, survival, and differentiation of neural progenitor cells provides interesting prospects for long-term neural repair after acute brain damage.

The endocannabinoid system has been involved in the modulation of neural stem cells proliferation, survival and differentiation as well as in the generation of new oligodendrocyte progenitors in the postnatal brain. The present work aims to test the effect of the synthetic Type 1 and Type 2 cannabinoid receptor agonist WIN55212-2 on these processes in the context of neonatal rat brain hypoxia–ischemia (HI)…

Our results suggest that the activation of the endocannabinoid system promotes white and gray matter recovery after neonatal HI injury…

In conclusion, we have demonstrated that the synthetic cannabinoid WIN55212-2 enhances SVZ cell proliferation, oligodendrogenesis, white matter remyelination, and neuroblast generation after neonatal HI.

These findings, summed to the previously described neuroprotective properties of cannabinoids after acute brain damage, may possess therapeutic repercussions in the long-term management of neonatal HI encephalopathy, a prevalent and devastating condition for which no pharmacological treatments are yet available.”

http://stroke.ahajournals.org/content/41/12/2956.full

 

Cannabis may help stroke recovery

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“CANNABIS may help to reduce brain damage after a stroke, new research suggests.

Chemical compounds found in the plant could help shrink the area of the brain affected by stroke, the study says.

Cannabinoids in the plant, as well as those that can be made artificially and those found naturally in the body, can also help improve brain function after a stroke attack, the authors said.

The study, which is to be presented to the annual UK Stroke Forum, examined previous studies conducted on the effect of the compound.

The authors, from the University of Nottingham, examined 94 studies evaluating the effects of cannabinoids on 1022 male rats, mice or monkeys.

They say the chemical “shows promise as a neuroprotective treatment for stroke”.

“This meta-analysis of pre-clinical stroke studies provides valuable information on the existing, and importantly, missing data on the use of cannabinoids as a potential treatment for stroke patients,” said lead author Dr Tim England, honorary consultant stroke physician at the University of Nottingham and Royal Derby Hospital.

Dr Dale Webb, director of research and information at the Stroke Association, added: “Stroke is the leading cause of adult disability in the UK, with more than half of all stroke survivors left dependent on others for everyday activities. With more people in the UK surviving a stroke, it’s never been more important to find new treatments to help more stroke patients make better recoveries.

“This new research is an example of the many new developments in the field of stroke which are being presented at this year’s UK Stroke Forum.

“The findings have identified the potential for cannabinoids to reduce brain damage caused by stroke.”

http://www.news.com.au/world/breaking-news/cannabis-may-help-stroke-recovery/story-e6frfkui-1226774100340

Chemicals in Marijuana May Help Stroke Victims

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NewsBriefs

“Scientists at the National Institute of Mental Health (NIMH) said a chemical in marijuana may protect the brain from damage inflicted by a stroke.

Their study was reported in the Proceedings of the National Academy of Sciences (Aidan Hampson, et al., “Cannabidiol and Delta-9-tetrahydrocannabinol Are Neuroprotective Antioxidants,” Proceedings of the National Academy of Sciences, July 7, 1998, Vol. 95, Issue 14, p. 8268; “Pot Chemicals Might Inhibit Breast Tumors, Stroke Damage,” Dallas Morning News, July 13, 1998; Vanessa Thorpe, “Chemicals Help Brain Damage After Stroke,” The Independent (UK), July 19, 1998).

NIMH scientists researched the effects of two cannabinoids, cannabidiol and THC, on the brains of rats. THC is the ingredient in marijuana that causes a psychoactive effect. However, cannabidiol is “a better candidate,” in part, because it does not cause a “high” in the patient, said Aidan Hampson, a neuropharmacologist at NIMH who led the study.

The cannabinoids block a neurochemical, known as glutamate, that leads to the formation of toxic oxidizing molecules that kill brain cells. Glutamate is produced in the brain if the oxygen supply is cut off, for example, as the result of blood clot leading to a stroke.

Researchers found that cannabidiol is a more effective antioxidant than vitamins A and E, which already are known to block the damaging effects of glutamate.”

http://www.ndsn.org/julaug98/medmj1.html

CB2 cannabinoid receptors as an emerging target for demyelinating diseases: from neuroimmune interactions to cell replacement strategies

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Figure 2

“Amongst the various demyelinating diseases that affect the central nervous system, those induced by an inflammatory response stand out because of their epidemiological relevance. The best known inflammatory-induced demyelinating disease is multiple sclerosis, but the immune response is a common pathogenic mechanism in many other less common pathologies (e.g., acute disseminated encephalomyelitis and acute necrotizing haemorrhagic encephalomyelitis).

In all such cases, modulation of the immune response seems to be a logical therapeutic approach.

Cannabinoids are well known immunomodulatory molecules that act through CB1 and CB2 receptors. While activation of CB1 receptors has a psychotropic effect, activation of CB2 receptors alone does not. Therefore, to bypass the ethical problems that could result from the treatment of inflammation with psychotropic molecules, considerable effort is being made to study the potential therapeutic value of activating CB2 receptors.

In this review we examine the current knowledge and understanding of the utility of cannabinoids as therapeutic molecules for inflammatory-mediated demyelinating pathologies. Moreover, we discuss how CB2 receptor activation is related to the modulation of immunopathogenic states.

The activation of CB2receptors results in the modulation of the inflammatory response, restraining one of the agents responsible for the progress of demyelination and neuronal death, the ultimate causes of the symptoms in pathologies such as MS and EAE.

The modulation of inflammatory molecules through CB2 receptors could also enhance remyelination, stimulating the survival of oligodendrocyte precursors and neural stem/precursor cells, and their development into mature oligodendrocytes.

…this raises the possibility that CB2 agonists could have the potential to promote brain repair.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219542/#!po=48.0769

Multiple sclerosis may disrupt endocannabinoid brain protection mechanism

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“Since the discovery of the endocannabinoids [eCB; anandamide and 2-arachidonoylglycerol (2-AG), various pathological conditions were shown to increase the eCB tone and to inhibit molecular mechanisms that are involved in the production, release, and diffusion of harmful mediators such as proinflammatory cytokines or excess glutamate.

In this issue of PNAS, Witting et al.  demonstrate that, unexpectedly and contrary to the effects of other brain diseases, cell damage induced by experimental autoimmune encephalomyelitis (EAE), an immune-mediated disease widely used as a laboratory model of multiple sclerosis (MS), does not lead to enhancement of eCB levels, although the cannabinoid receptors remain functional.

Nearly two decades ago, Lyman et al.  reported that Δ9-THC, the psychoactive component of marijuana, suppresses the symptoms of EAE. A few years later, Wirguin et al. reported the same effect by Δ8-THC, a more stable and less psychotropic analogue of Δ9-THC.

Thus, THC was shown to inhibit both clinical and histological signs of EAE even before the endocannabinoids were described.

THC was also shown to control spasticity and tremor in chronic relapsing EAE, a further autoimmune model of MS , and to inhibit glutamate release via activation of the CB1-cannabinoid receptor in EAE. Moreover, mice deficient in the cannabinoid receptor CB1 tolerate inflammatory and excitotoxic insults poorly and develop substantial neurodegeneration after immune attack in EAE.

Thus, the brain loses some of its endogenous neuroprotective capacity, but it may still respond to exogenous treatment with 2-AG or other CB1 agonists. Assuming that the biochemical changes taking place in the EAE model of MS are similar to those in MS itself, these results represent a biochemical-based support to the positive outcome noted with cannabinoid therapy in MS.

These data suggest that the high level of IFN-γ in the CNS, noted in mice with EAE, disrupts eCB-mediated neuroprotection, while maintaining functional cannabinoid receptors, thus providing additional support for the use of cannabinoid-based medicine to treat MS.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1458835/

Cannabidiol: Pharmacology and potential therapeutic role in epilepsy and other neuropsychiatric disorders.

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“Cannabis has been used to treat disease since ancient times. Δ9 -Tetrahydrocannabinol (Δ9 -THC) is the major psychoactive ingredient and CBD is the major nonpsychoactive ingredient in cannabis.

Cannabis and Δ9 -THC are anticonvulsant in most animal models but can be proconvulsant in some healthy animals. The psychotropic effects of Δ9 -THC limit tolerability.

CBD is anticonvulsant in many acute animal models, but there are limited data in chronic models.

The antiepileptic mechanisms of CBD are not known, but may include effects on the equilibrative nucleoside transporter; the orphan G-protein-coupled receptor GPR55; the transient receptor potential of vanilloid type-1 channel; the 5-HT1a receptor; and the α3 and α1 glycine receptors.

CBD has neuroprotective and antiinflammatory effects, and it appears to be well tolerated in humans, but small and methodologically limited studies of CBD in human epilepsy have been inconclusive.

More recent anecdotal reports of high-ratio CBD:Δ9 -THC medical marijuana have claimed efficacy, but studies were not controlled.

CBD bears investigation in epilepsy and other neuropsychiatric disorders, including anxiety, schizophrenia, addiction, and neonatal hypoxic-ischemic encephalopathy.”

http://www.ncbi.nlm.nih.gov/pubmed/24854329