Cannabidiol inhibits inducible nitric oxide synthase protein expression and nitric oxide production in beta-amyloid stimulated PC12 neurons through p38 MAP kinase and NF-kappaB involvement.

“In view of the pro-inflammatory scenario observed in Alzheimer’s disease, in the recent years anti-inflammatory drugs have been proposed as potential therapeutic agents. We have previously shown that cannabidiol, the main non-psychotropic component from Cannabis sativa, possess a variegate combination of anti-oxidant and anti-apoptotic effects that protect PC12 cells from Abeta toxicity. In parallel, cannabidiol has been described to have anti-inflammatory properties in acute models of inflammation …

The here reported data increases our knowledge about the possible neuroprotective mechanism of cannabidiol, highlighting the importance of this compound to inhibit beta-amyloid induced neurodegeneration, in view of its low toxicity in humans.”

http://www.ncbi.nlm.nih.gov/pubmed/16490313

Effects of cannabinoids on the immune system and central nervous system: therapeutic implications.

“Cannabinoids possess immunomodulatory activity, are neuroprotective in vivo and in vitro and can modify the production of inflammatory mediators… Cannabinoid-induced immunosuppression may have implications for the treatment of neurological disorders that are associated with excess immunological activity, such as multiple sclerosis and Alzheimer’s disease. There is anecdotal evidence that cannabis use improves the symptoms of multiple sclerosis, and studies with animal models are beginning to provide evidence for the mechanism of such effects. The development of nonpsychotropic cannabinoid analogues and modulators of the metabolism of endogenous cannabinoid ligands may lead to novel approaches to the treatment of neurodegenerative disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/18031185

Microglial interaction with beta-amyloid: implications for the pathogenesis of Alzheimer’s disease.

Abstract

“The etiology of Alzheimer’s disease (AD) involves a significant inflammatory component as evidenced by the presence of elevated levels of a diverse range of proinflammatory molecules in the AD brain. These inflammatory molecules are produced principally by activated microglia, which are found to be clustered within and adjacent to the senile plaque. Moreover, long-term treatment of patients with non-steroidal anti-inflammatory drugs has been shown to reduce risk and incidence of AD and delay disease progression. The microglia respond to beta-amyloid (Abeta) deposition in the brain through the interaction of fibrillar forms of amyloid with cell surface receptors, leading to the activation of intracellular signal transduction cascades. The activation of multiple independent signaling pathways ultimately leads to the induction of proinflammatory gene expression and production of reactive oxygen and nitrogen species. These microglial inflammatory products act in concert to produce neuronal toxicity and death. Therapeutic approaches focused on inhibition of the microglial-mediated local inflammatory response in the AD brain offer new opportunities to intervene in the disease.”

http://www.ncbi.nlm.nih.gov/pubmed/11455613

In search of a treatment for Alzheimer’s disease and potential immunonosuppresive therapeutic interventions.

Abstract

“Alzheimer’s disease (AD) is a serious neurodegenerative disease of aging. Recent projections of the dramatic increase in AD incidence worldwide by 2050 reveal its magnitude as a world-wide health crisis and underscore the urgent need to understand the etiology of AD in order to develop therapeutic interventions. A popular debate among scientists has traditionally pitted those in support of Beta amyloid protein as a causative factor (“Baptists”) against others who implicate tau hyperphosphorylation (“Tauists”). Considering the significance of Beta amyloid protein and hyperphosphorlyated tau protein aggregates in AD pathology, this article delves into the nature of inflammation associated with these aggregates. Aspects of inflammation focus on microglia, resident immune cells of the CNS that are activated during AD inflammation and are known to play a significant role in pathogenesis. This article discusses the role of microglia, inflammation, and the immune response as a middle ground in the debate between the “Tauists” and the “Baptists” respective positions. It explores recent advances in immunotherapy and supports continued research in and use of immunosuppressive regimens as potential therapeutic interventions for AD.”

http://www.ncbi.nlm.nih.gov/pubmed/18766151

Cannabis May Cut Alzheimer’s Risk – Discovery News

“For those who have inhaled, there may be some good news: Marijuana use may cut the risk of developing Alzheimer’s disease by reducing inflammation in the brain…

The findings may explain studies showing those who regularly used marijuana in the 1960s and 1970s are now less likely to develop Alzheimer’s disease than their non-smoking contemporaries.

Under a National Institutes of Health grant, researchers used a synthetic drug similar to marijuana to treat rats with brain inflammation typically associated with Alzheimer’s disease, a form of dementia that afflicts 4.5 million people in the United States alone.”

Read more: http://dsc.discovery.com/news/2006/10/19/marijuana_hea.html

Marijuana Ingredient May Help Alzheimer’s – WebMD

“Chemical Counters Brain Problems in Alzheimer’s Disease, Says Spanish Study.
New clues about Alzheimer’s disease have emerged from a Spanish study of marijuana. The drug’s active ingredients — cannabinoids — help prevent brain problems seen in Alzheimer’s, say the scientists.

The findings showed that “cannabinoids work both to prevent inflammation and to protect the brain,” says researcher Maria de Ceballos in a news release. That “may set the stage for [cannabinoids’] use as a therapeutic approach for [Alzheimer’s disease].”

The cannabinoids completely prevented activation of cells that trigger inflammation. These cells gather near plaque and are believed to be involved in the development of Alzheimer’s disease.

“Our results indicate that cannabinoid receptors are important in the pathology of Alzheimer’s disease and that cannabinoids succeed in preventing the neurodegenerative process occurring in the disease,” write the researchers in the journal.”

Read more: http://www.webmd.com/alzheimers/news/20050223/marijuana-ingredient-may-help-alzheimers

Marijuana Ingredient May Help Alzheimer’s – FoxNews

“New clues about Alzheimer’s disease have emerged from a Spanish study of marijuana. The drug’s active ingredients — cannabinoids — help prevent brain problems seen in Alzheimer’s, say the scientists. 

The new study didn’t test cannabinoids on people living with Alzheimer’s disease. Instead, the researchers focused on human brain tissue samples and conducted cannabinoid experiments on rats. 

The findings showed that “cannabinoids work both to prevent inflammation and to protect the brain,” says researcher Maria de Ceballos in a news release. That “may set the stage for [cannabinoids’] use as a therapeutic approach for [Alzheimer’s disease].””

Read more: http://www.foxnews.com/story/0,2933,148518,00.html

Read more: http://www.foxnews.com/story/0,2933,148518,00.html#ixzz2HIrp1uDH

Marijuana May Slow Alzheimer’s Memory Loss

“New evidence from animal models suggests marijuana may contain compounds that slow the memory loss associated with Alzheimer’s disease. Older rats treated with a synthetic chemical similar to marijuana significantly improved their ability to navigate a maze. Researchers believe the strong anti-inflammatory effects of marijuana slow Alzheimer’s progression.”

marijuanaleaves

“The link between chronic inflammation and the progression of Alzheimer’s is compelling, said Gary Wenk, a study co-author and a professor of psychology at Ohio State University.

“Inflammation in the brain is part of aging,” Wenk said. “It happens to almost all of us as we age. But in some cases, this inflammation gets out of hand and causes serious damage.”

Treatment with a synthetic compound similar to marijuana reduced inflammation in older rats in addition to making the animals “smarter,” said Wenk, who is also a professor of neuroscience and molecular virology, immunology and medical genetics.

“The compound substantially improved the memories of the older rats,” he said. “These animals were able to hold on to key details of a specific task. Untreated older rats, on the other hand, were not.”

The researchers presented their findings at the annual Society for Neuroscience meeting.

Evidence suggests that people who regularly smoked marijuana in the 1960s and 1970s rarely develop Alzheimer’s disease, said Wenk, adding that researchers are eager to develop a drug with the anti-inflammatory properties of marijuana, but without the drug’s psychoactive effects.”

Read more: http://psychcentral.com/news/2006/10/23/marijuana-may-slow-alzheimers-memory-loss/350.html

The therapeutic potential of the endocannabinoid system for Alzheimer’s disease.

“Based on the complex pathology of AD, a preventative, multimodal drug approach targeting a combination of pathological AD symptoms appears ideal. Importantly, cannabinoids show anti-inflammatory, neuroprotective and antioxidant properties and have immunosuppressive effects. Thus, the cannabinoid system should be a prime target for AD therapy. The cannabinoid receptor 2 appears to be a promising candidate but its role in AD has to be investigated cautiously. Furthermore, the phytocannabinoid cannabidiol is of particular interest as it lacks the psychoactive and cognition-impairing properties of other cannabinoids. In conclusion, future research should focus on the evaluation of the effects of manipulations to the endocannabinoid system in established animal models for AD, combined with early-phase studies in humans.”

http://www.ncbi.nlm.nih.gov/pubmed/22448595

Scientists are high on idea that marijuana reduces memory impairment

“The more research they do, the more evidence Ohio State University scientists find that specific elements of marijuana can be good for the aging brain by reducing inflammation there and possibly even stimulating the formation of new brain cells.

The research suggests that the development of a legal drug that contains certain properties similar to those in marijuana might help prevent or delay the onset of Alzheimer’s disease. Though the exact cause of Alzheimer’s remains unknown, chronic inflammation in the brain is believed to contribute to memory impairment.

Any new drug’s properties would resemble those of tetrahydrocannabinol, or THC, the main psychoactive substance in the cannabis plant, but would not share its high-producing effects.

.”Could people smoke marijuana to prevent Alzheimer’s disease if the disease is in their family? We’re not saying that, but it might actually work. What we are saying is it appears that a safe, legal substance that mimics those important properties of marijuana can work on receptors in the brain to prevent memory impairments in aging. So that’s really hopeful,” Wenk said”

Read more: http://phys.org/news146320102.html