Cannabis may help reverse dementia: study

Cannabis may help reverse dementia: study

Cannabis may help reverse dementia: study

Date
February 6, 2013

Amy Corderoy
Amy Corderoy
Health Editor, Sydney Morning Herald

View more articles from Amy Corderoy

It makes most people a little foggy-headed, but scientists are investigating whether an active ingredient in cannabis could actually stave off dementia.

A team from Neuroscience Research Australia is in the early stages of research examining if one of the main active ingredients in cannabis, called cannabidiol, could reverse some of the symptoms of memory loss in animals.

Tim Karl, a senior research fellow with the group, said cannabidiol does not have the same psychoactive effects as the main component of marijuana, THC, but it has been found to have anti-inflammatory, antioxidant and other effects that could be beneficial for the brain.

“Back in the day cannabis was used for medical purposes, I'm talking 200 years, 100 years back, then at some point people discovered it had other effects and, as quite often happens in our society, people decided it was a bad drug,” he said.
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“But it's not one compound, it is a mixture of 60 different compounds, and you just have to look at those different compounds because some of them might be good for you.”

His study involved injecting cannabidiol into mice that had been bred to have similar symptoms as those seen in Alzheimer's, as well as examining what would happen to brain cells treated with the drug.

Dr Karl found that when the mice were given the cannabidiol they showed drastic improvement on parts of the tests that were related to recognising and remembering objects and other mice.

“It basically brings the performance of the animals back to the level of healthy animals,” he said. “You could say it cured them, but we will have to go back and look at their brains to be sure.”

The study was done as part of the PhD of student David Cheng, who has also collected the brains of the mice and intends to examine them to see if they showed physical improvements.

As part of the research, which is being presented at the Australian Neuroscience Society annual meeting in Melbourne this week, the team also treated animal brain cells that produced a protein linked to the development of plaques in the brain in humans with Alzheimer's disease, amyloid precursor protein.

The cell research, done at the University of Wollongong, found treating the cells with cannabidiol also reduced the amount of the harmful protein that they produced.

Dr Karl said there had been case reports in medical literature of marijuana smokers who had developed Alzheimer's disease, only to find their smoking seemed to relieve some of their symptoms.

“Most of the components [of marijuana] are detrimental, they worsen your cognitive performance and have psychoactive effects… cannabidiol seems to not have any of these negative effects,” he said.

http://www.smh.com.au/national/cannabis-may-help-reverse-dementia-study-20130206-2dxsk.html#ixzz2j49Wiotc

Cannabinoids Destroy Leukemia Cells, New Study Finds

14 October 2013 St George's, University of London

New research has shown that the non-hallucinogenic components of cannabis could act as effective anti-cancer agents.
The anti-cancer properties of tetrahydrocannabinol (THC), the primary hallucinogenic component of cannabis, has been recognised for many years, but research into similar cannabis-derived compounds, known as cannabinoids, has been limited.
The study was carried out by a team at St George’s, University of London. It has been published in the journal Anticancer Research.
The team, led by Dr Wai Liu and colleagues carried out laboratory investigations using a number of cannabinoids, either alone or in combination with each other, to measure their anti-cancer actions in relation to leukaemia.
Of six cannabinoids studied, each demonstrated anti-cancer properties as effective as those seen in THC. Importantly, they had an increased effect on cancer cells when combined with each other.
Dr Liu said: “This study is a critical step in unpicking the mysteries of cannabis as a source of medicine. The cannabinoids examined have minimal, if any, hallucinogenic side effects, and their properties as anti-cancer agents are promising.
“These agents are able to interfere with the development of cancerous cells, stopping them in their tracks and preventing them from growing. In some cases, by using specific dosage patterns, they can destroy cancer cells on their own.
“Used in combination with existing treatment, we could discover some highly effective strategies for tackling cancer. Significantly, these compounds are inexpensive to produce and making better use of their unique properties could result in much more cost effective anti-cancer drugs in future.”
This latest research is part of a growing portfolio of studies into the medicinal properties of cannabis by the research team at St George’s. The next step will be to examine in the laboratory these compounds in combination with existing anti-cancer treatments and study treatment schedules to identify strategies that will maximise their efficacy.
The study examined two forms of cannabidiol (CBD), two forms of cannabigerol (CBG) and two forms of cannabigevarin (CBGV). These represent the most common cannabinoids found in the cannabis plant apart from THC.
http://ar.iiarjournals.org/content/33/10/4373.abstract

THC Cannabinoid Helpful in Treatment of Parkinson’s

Posted October 12th, 2013 by Monterey Bud & filed under marijuana research, marijuana studies.

Add this November 2013 report – soon to be published in the Journal of Neurology, Neurosurgery & Psychiatry  (in next month’s hard copy issue) – to the long list of scientific research, documenting marijuana’s THC cannabinoid as  demonstrating remarkable positive medicinal effects. Already accessible to the public,  the National Institute of Health was the first to disseminate the report online:

“Δ9-TETRAHYDROCANNABINOL IS PROTECTIVE THROUGH PPARγ DEPENDENT MITOCHONDRIAL BIOGENESIS IN A CELL CULTURE MODEL OF PARKINSON’S DISEASE.”

Abstract

INTRODUCTION:

Cannabinoids such as Δ9-tetrahydrocannabinol (Δ9-THC) are neuroprotective in animal and cell culture models of Parkinson’s disease (PD). In a PD cell culture model we recently demonstrated that Δ9-THC is neuroprotective through activation of the nuclear receptor peroxisomal proliferator-activated receptor γ (PPARγ). Furthermore, activation by specific agonists rosiglitazone and pioglitazone, has also been found neuroprotective. PPARγ is a nuclear receptor whose activation can lead to the expression of proteins involved in the de novo synthesis of mitochondria. One such protein is the PPARγ co-activator 1 α (PGC1α) as it co-activates NRF-1 mediated gene expression which is essential for the production of nuclear encoded, mitochondrial proteins. Here we investigate the effect of Δ9-THC and pioglitazone on mitochondrial biogenesis.

METHODS:

SH-SY5Y neuroblastoma cells were differentiated with retinoic acid and exposed to the PD relevant mitochondrial complex 1 inhibitor, MPP+. Δ9-THC and pioglitazone were co-administered with the minimum concentration of the specific PPARγ antagonist T0070907 able to block the protective effect of each compound respectively for 48 hours. The production of reactive oxygen species was then measured, proteins were extracted for Western blotting and total DNA was extracted to determine mitochondrial DNA (mtDNA) content by QPCR.

RESULTS:

Δ9-THC resulted in significant inhibition of MPP+ induced oxidative stress which was completely reversed by T0070907 whereas pioglitazone induced reduction in oxidative stress did not seem to be PPARγ dependent. Accordingly, both pioglitazone and Δ9-THC were able to restore MPP+ induced down-regulation of PGC1α, to the level of untreated control. This effect was inhibited by T0070907 in the case of Δ9-THC but not pioglitazone. Whilst NRF1 expression remained unaffected by all treatments, the mitochondrial transcription factor (tfam) which is necessary for mtDNA replication was reduced with MPP+ and up-regulated by Δ9-THC only. Similarly, mtDNA content and the mitochondrial marker COX4 were only increased by Δ9-THC.

CONCLUSIONS:

Even though Δ9-THC and pioglitazone are both protective against MPP+ only Δ9-THC induces PPARγ dependent mitochondrial biogenesis, a mechanism that may be beneficial for the treatment of PD.