Cannabis May Offer Alzheimer’s Hope, Study Says

“Marijuana compounds offer an alternative approach for treating the neurodegeneration associated with Alzheimer’s disease (AD)…

Investigators at the Trinity College, Institute for Neuroscience, in Dublin report that cannabinoids have been shown to protect neurons from the deleterious effects of amyloid plaque – the primary pathological hallmark of Alzheimer’s. Cannabinoids also demonstrate a propensity to reduce oxidative stress and inflammation, while also promoting neurogenesis (the birth of new neuronal cells), authors report.

Authors write: “In recent years the proclivity of cannabinoids to exert a neuroprotective influence has received substantial interest as a means to mitigate the symptoms of neurodegenerative conditions. … [C]annabinoids offer a multi-faceted approach for the treatment of Alzheimer’s disease by providing neuroprotection and reducing neuroinflammation, whilst simultaneously supporting the brain’s intrinsic repair mechanisms by augmenting neurotrophin expression and enhancing neurogenesis. … Manipulation of the cannabinoid pathway offers a pharmacological approach for the treatment of AD that may be efficacious than current treatment regimens.”

Preclinical studies have demonstrated that cannabinoids can delay disease progression in animal models of several neurodegenerative diseases, including multiple sclerosis and amyotrophic lateral sclerosis (Lou Gehrig’s disease).”-

Paul Armentano, NORML  http://norml.org/news/2007/09/20/cannabis-may-offer-alzheimers-hope-study-says

Full text of the study, “Alzheimer’s disease; taking the edge off with cannabinoids?” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190031/

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Scientists claim cannabis can offer hope for Alzheimer’s sufferers

“New cannabis-based treatments could improve memory loss in Alzheimer’s sufferers, scientists claim.

One of the 400 compounds in the drug can significantly slow memory problems caused by the disease, tests show.”

Read more: http://www.dailymail.co.uk/health/article-530252/Scientists-claim-cannabis-offer-hope-Alzheimers-sufferers.html#ixzz2HOpZYThw

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Marijuana May Slow Alzheimer’s – WebMD

“Key Marijuana Compound Beats Current Alzheimer’s Drugs in Test-Tube Study.
THC, the key compound in marijuana, may also be the key to new drugs for Alzheimer’s disease.”While we are certainly not advocating the use of illegal drugs, these findings offer convincing evidence that THC possesses remarkable inhibitory qualities, especially when compared to [Alzheimer’s drugs] currently available to patients,” Janda says in a news release.

“Although our study is far from final, it does show that there is a previously unrecognized molecular mechanism through which THC may directly affect the progression of Alzheimer’s disease.”

“THC and its analogs may provide an improved [treatment for] both the symptoms and progression of Alzheimer’s disease,” the researchers conclude”

Read more: http://www.webmd.com/alzheimers/news/20061006/marijuana-may-slow-alzheimers

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Marijuana may help stave off Alzheimer’s – NBCNews

“Active ingredient in pot may help preserve brain function.

Good news for aging hippies: smoking pot may stave off Alzheimer’s disease.

New research shows that the active ingredient in marijuana may prevent the formation of deposits in the brain associated with the degenerative disease.

Researchers at the Scripps Research Institute in California found that marijuana’s active ingredient, delta-9-tetrahydrocannabinol, or THC, can prevent an enzyme called acetylcholinesterase from accelerating the formation of “Alzheimer plaques” in the brain more effectively than commercially marketed drugs.

THC is also more effective at blocking clumps of protein that can inhibit memory and cognition in Alzheimer’s patients, the researchers reported in the journal Molecular Pharmaceutics.

The researchers said their discovery could lead to more effective drug treatment for Alzheimer’s, the leading cause of dementia among the elderly.

Those afflicted with Alzheimer’s suffer from memory loss, impaired decision-making, and diminished language and movement skills. The ultimate cause of the disease is unknown, though it is believed to be hereditary.

Marijuana is used to relieve glaucoma and can help reduce side effects from cancer and AIDS treatment.”

http://www.msnbc.msn.com/id/15145917/ns/health-alzheimers_disease/t/marijuana-may-help-stave-alzheimers/

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Marijuana May Slow Alzheimer’s – CBSNews

“THC, the key compound in marijuana, may also be the key to new drugs for Alzheimer’s disease. That’s because the marijuana compound blocks the formation of brain-clogging Alzheimer’s plaques better than current Alzheimer’s drugs….
 these findings offer convincing evidence that THC possesses remarkable inhibitory qualities, especially when compared to [Alzheimer’s drugs] currently available to patients,” Janda says in a news release.

“Although our study is far from final, it does show that there is a previously unrecognized molecular mechanism through which THC may directly affect the progression of Alzheimer’s disease.”

Janda’s team found that THC blocks an enzyme called acetylcholinesterase, which speeds the formation of amyloid plaque in the brains of people with Alzheimer’s disease.

The Alzheimer’s drugs Aricept and Cognex work by blocking acetylcholinesterase. When tested at double the concentration of THC, Aricept blocked plaque formation only 22 percent as well as THC, and Cognex blocked plaque formation only 7 percent as well as THC.

“THC and its analogs may provide an improved [treatment for] both the symptoms and progression of Alzheimer’s disease,” the researchers conclude.”

Read more: http://www.cbsnews.com/2100-500368_162-2072101.html

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Cannabinoid receptor signalling in neurodegenerative diseases: a potential role for membrane fluidity disturbance

Abstract

“Type-1 cannabinoid receptor (CB1) is the most abundant G-protein-coupled receptor (GPCR) in the brain. CB1 and its endogenous agonists, the so-called ‘endocannabinoids (eCBs)’, belong to an ancient neurosignalling system that plays important functions in neurodegenerative and neuroinflammatory disorders like Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and multiple sclerosis. For this reason, research on the therapeutic potential of drugs modulating the endogenous tone of eCBs is very intense. Several GPCRs reside within subdomains of the plasma membranes that contain high concentrations of cholesterol: the lipid rafts. Here, the hypothesis that changes in membrane fluidity alter function of the endocannabinoid system, as well as progression of particular neurodegenerative diseases, is described. To this end, the impact of membrane cholesterol on membrane properties and hence on neurodegenerative diseases, as well as on CB1 signalling in vitro and on CB1-dependent neurotransmission within the striatum, is discussed. Overall, present evidence points to the membrane environment as a critical regulator of signal transduction triggered by CB1, and calls for further studies aimed at better clarifying the contribution of membrane lipids to eCBs signalling. The results of these investigations might be exploited also for the development of novel therapeutics able to combat disorders associated with abnormal activity of CB1.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165948/

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Cannabinoid receptor stimulation is anti-inflammatory and improves memory in old rats

“The number of activated microglia increase during normal aging. Stimulation of endocannabinoid receptors can reduce the number of activated microglia, particularly in the hippocampus, of young rats infused chronically with lipopolysaccharide (LPS). In the current study we demonstrate that endocannabinoid receptor stimulation by administration of WIN-55212-2 (2 mg/kg/day) can reduce the number of activated microglia in hippocampus of aged rats and attenuate the spatial memory impairment in the water pool task. Our results suggest that the action of WIN-55212-2 does not depend upon a direct effect upon microglia or astrocytes but is dependent upon stimulation of neuronal cannabinoid receptors. Aging significantly reduced cannabinoid type 1 receptor binding but had no effect on cannabinoid receptor protein levels. Stimulation of cannabinoid receptors may provide clinical benefits in age-related diseases that are associated with brain inflammation, such as Alzheimer’s disease.”

“Our results are consistent with the hypothesis that CB receptors on hippocampal neurons modulate glutamatergic and GABAergic function and this leads to reduced microglia activation. This mechanism may underlie the neuroprotective effects of cannabinoids”.

“Importantly, the benefits of cannabinoid receptor stimulation occurred at a dose that did not impair performance in a spatial memory task, indeed the performance of aged rats was significantly improved. This finding is particularly relevant for elderly for patients suffering with diseases associated with brain inflammation, e.g. AD, Parkinson’s disease or multiple sclerosis. The current report is the first to our knowledge to demonstrate the anti-inflammatory actions of cannabinoid therapy in aged animals and strongly advocate an cannabinoid-based therapy for neuroinflammation-related diseases, as well as a potential tool to reduce the impairment in memory processes occurring during normal aging.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586121/

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Can the benefits of cannabinoid receptor stimulation on neuroinflammation, neurogenesis and memory during normal aging be useful in AD prevention?

Abstract

“Background

Alzheimer’s disease has become a growing socio-economical concern in developing countries where increased life expectancy is leading to large aged populations. While curing Alzheimer’s disease or stopping its progression does not appear within reach in a foreseeable future, new therapies capable of delaying the pathogenesis would represent major breakthroughs.

Presentation of the hypothesis

The growing number of medical benefits of cannabinoids, such as their ability to regulate age-related processes like neuroinflammation, neurogenesis and memory, raise the question of their potential role as a preventive treatment of AD.

Testing the hypothesis

To test this hypothesis, epidemiological studies on long term, chronic cannabinoid users could enlighten us on the potential benefits of these compounds in normal and pathological ageing processes. Systematic pharmacological (and thus more mechanistic) investigations using animal models of Alzheimer’s disease that have been developed would also allow a thorough investigation of the benefits of cannabinoid pharmacotherapy in the pathogenesis of Alzheimer’s disease.

Implications of the hypothesis

The chronic administration of non-selective cannabinoids may delay the onset of cognitive deficits in AD patients; this will dramatically reduce the socio-economic burden of AD and improve the quality of life of the patients and their families.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3284401/

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Anti-inflammatory property of the cannabinoid agonist WIN-55212-2 in a rodent model of chronic brain inflammation

“Cannabinoid receptors (CBr) stimulation induces numerous central and peripheral effects. A growing interest in the beneficial properties of manipulating the endocannabinoid system has lead to the possible involvement of CBr in the control of brain inflammation… Our results emphasize the potential use of CBr agonists in the regulation of inflammatory processes within the brain; this knowledge may lead to the use of CBr agonists in the treatment of neurodegenerative diseases associated with chronic neuroinflammation, such as Alzheimer disease.”

“The current report is the first to our knowledge to demonstrate the modulatory role of cannabinoids in an animal model of chronic neuroinflammation, pointing out the effectiveness of a CBr agonist on the consequences of LPS mediated neuroinflammation at a dose (0.5 mg/kg/day i.p. of WIN-55212-2) that does not impair performance in a patial memory task. These results further advocate for the manipulation of the endocannabinoid system to diminish the consequences of neuroinflammation in progression of AD and others inflammation-related diseases.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1852513/

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Inflammation and aging: can endocannabinoids help?

“Aging often leads to cognitive decline due to neurodegenerative process in the brain. As people live longer, a growing concern exist linked to long-term, slowly debilitating diseases that have not yet found a cure, such as Alzheimer’s disease. Recently, the role of neuroinflammation has attracted attention due to its slow onset, chronic nature and its possible role in the development of many different neurodegenerative diseases. In the future, treatment of chronic neuroinflammation may help counteract aspects of neurodegenerative disease. Our recent studies have focused upon the endocannabinoid system for its unique effects on the expression of neuroinflammation. The basis for the manipulation of the endocannabinoid system in the brain in combination with existing treatments for Alzheimer’s disease will be discussed in this review.”

“Endocannabinoids

Cannabinoid refers to naturally occurring or synthetic molecules mimicking the activity of plant-derived cannabinoids from Cannabis Sativa. Two types of cannabinoid receptors have been so far identified in the body, named CB1 and CB2. Discovery of cannabinoid receptors (CBr) lead to the finding of endogenous agonists for these receptors called endocannabinoids (EC). EC are derived from arachidonic acid, arachidonoylethanolamide (anandamide), and 2-arachidonoyl glycerol (2-AG), synthesized on-demand post-synaptically and released in response to the entry of calcium ions. These EC in combination with the two known CBr constitute the endocannabinoid system (ECS). In the central nervous system (CNS), CB1 is overwhelmingly represented over CB2 and particularly abundant in cortical regions, the hippocampus, cerebellum and basal ganglia while CB2 may be restricted to microglia or neurons in the brainstem  and cerebellum. Deactivation of the EC is due to a rapid enzymatic degradation in the synaptic cleft or after membrane transport. The ECS is thought to be a neuromodulator and an immunomodulator. In the CNS, the ECS can influence food intake, endocrine release, motor control, cognitive processes, emotions and perception. Cannabinoids treatment has been shown to be neuroprotective under many experimental conditions. Drugs that manipulate the ECS are currently evaluated in various diseases ranging from cancer to AIDS for their peripheral analgesic and immunosuppressive properties. Their anti-inflammatory actions may make them useful in the treatment of multiple sclerosis, Parkinson’s disease and AD. Very little in vivo evidence to support the use of EC receptor agonists has been reported, although in vitro studies have found evidence for their anti-inflammatory effectiveness. Our recent work demonstrated the anti-inflammatory effect of a chronic treatment of a low dose of the CBr agonist WIN-55,212-2 (without psychoactive effects) on the consequences of chronic neuroinflammation induced by the infusion of LPS into the 4th ventricle of young rats. Moreover, that same anti-inflammatory effect was found using a non-psychoactive dose given by slow subcutaneous infusion of WIN-55,212-2 to healthy aged rats; these rats also demonstrated improved spatial memory. Our ongoing work in aged rats has shown that treatment with the CBr agonist WIN-55,212-2 increases neurogenesis in the hippocampus. Our preliminary data suggest that the neurogenic and anti-inflammatory effects in aged rats are due to the agonist/antagonist properties of WIN-55,212-2 at multiple receptors.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408719/

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