Tag Archives: Alzheimer’s disease
CB(2) receptor and amyloid pathology in frontal cortex of Alzheimer’s disease patients.
“The cannabinoid system seems to play an important role in various neurodegenerative diseases including Alzheimer’s disease (AD). The relationship of cannabinoid receptors (CB(1)R and CB(2)R) to cognitive function and neuropathological markers in AD remains unclear. In the present study, postmortem cortical brain tissues (Brodmann area 10) from a cohort of neuropathologically confirmed AD patients and age-matched controls were used to measure CB(1)R and CB(2)R by immunoblotting. Correlational analyses were performed for the neurochemical and cognitive data. CB(1)R expression was significantly decreased in AD. Levels of CB(1)R correlated with hypophagia, but not with any AD molecular marker or cognitive status (Mini Mental State Examination score). The level of CB(2)R was significantly higher (40%) in AD. Increases in the expression of the glial marker glial fibrillar acidic protein were also found. CB(2)R expression did not correlate with cognitive status. Interestingly, expression levels of CB(2)R correlated with two relevant AD molecular markers, Aβ(42) levels and senile plaque score.
These results may constitute the basis of CB(2)R-based therapies and/or diagnostic approaches.”
Stimulation of cannabinoid receptor 2 (CB2) suppresses microglial activation
“Activated microglial cells have been implicated in a number of neurodegenerative disorders, including Alzheimer’s disease (AD), multiple sclerosis (MS), and HIV dementia. Many data reveal that cannabinoids mediate suppression of inflammation in vitro and in vivo through stimulation of cannabinoid receptor 2 (CB2).
Taken together, these results provide mechanistic insight into beneficial effects provided by cannabinoid receptor CB2 modulation in neurodegenerative diseases, particularly AD.”
Does Smoking Marijuana Prevent Alzheimer’s Disease?
“Maintaining Memories with Marijuana. Research in my laboratory has demonstrated that stimulating the brain’s marijuana receptors may offer protection by reducing brain inflammation and by restoring neurogenesis. Thus, later in life, marijuana might actually help your brain, rather than harm it.
It takes very little marijuana to produce benefits in the older brain; my colleague in France, Dr. Yannick Marchalant, coined the motto “a puff is enough” because it appears as though only a single puff each day is necessary to produce significant benefit.
The challenge for pharmacologists in the future will be to isolate the beneficial effects of the marijuana plant from its psychoactive effects.”
http://www.theweedblog.com/does-smoking-marijuana-prevent-alzheimers-disease/
Pot joins the fight against Alzheimer’s, memory loss
“The researchers ducked the obvious question of whether it might be simpler, faster and cheaper to simply light up a joint. “Could people smoke marijuana to prevent Alzheimer’s disease if the disease is in their family?” Wenk said in a statement. “We’re not saying that, but it might actually work.””
http://www.scientificamerican.com/blog/post.cfm?id=pot-joins-the-fight-against-alzheim-2008-11-19
Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression.
“Pharmacological inhibition of beta-amyloid (Aβ) induced reactive gliosis may represent a novel rationale to develop drugs able to blunt neuronal damage and slow the course of Alzheimer’s disease (AD). Cannabidiol (CBD), the main non-psychotropic natural cannabinoid, exerts in vitro a combination of neuroprotective effects in different models of Aβ neurotoxicity. The present study, performed in a mouse model of AD-related neuroinflammation, was aimed at confirming in vivo the previously reported antiinflammatory properties of CBD.
Cannabidiol (CBD), the main non-psychotropic component of the glandular hairs of Cannabis sativa, exhibits a plethora of actions including anti-convulsive, sedative, hypnotic, anti-psychotic, anti-nausea, anti-inflammatory and anti-hyperalgesic properties. CBD has been proved to exert in vitro a combination of neuroprotective effects in Aβ-induced neurotoxicity, including anti-oxidant and anti-apoptotic effects, tau protein hyperphosphorylation inhibition through the Wnt pathway, and marked decrease of inducible nitric oxide synthase (iNOS) protein expression and nitrite production in Aβ-challenged differentiated rat neuronal cells.
In spite of the large amount of data describing the significant neuroprotective and anti-inflammatory properties of CBD in vitro, to date no evidence has been provided showing similar effects in vivo. To achieve this, the present study investigated the potential anti-inflammatory effect of CBD in a mouse model of AD-related neuroinflammation induced by the intrahippocampal injection of the human Aβ (1–42) fragment.
The results of the present study confirm in vivo anti-inflammatory actions of CBD, emphasizing the importance of this compound as a novel promising pharmacological tool capable of attenuating Aβ evoked neuroinflammatory responses.
…on the basis of the present results, CBD, a drug well tolerated in humans, may be regarded as an attractive medical alternative for the treatment of AD, because of its lack of psychoactive and cognitive effects.”
Read more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189818/
Marijuana compound beats Alzheimer’s drugs in study
“THC, the key compound in marijuana, blocks the formation of brain-clogging plaques better than current Alzheimer’s drugs do. Medications like Aricept and Cognex work in much the same way as THC–by inhibiting the enzyme acetylcholinesterase–Researchers… point out that the compound THC… would likely be the key to developing new Alzheimer’s medications.”
Marijuana linked to preventing and treating Alzheimer’s disease
“Alzheimer’s disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer’s disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients as well as reduce the health care costs attributable to Alzheimer’s disease.
Here, we demonstrate that the active component of marijuana, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation, the key pathological marker of Alzheimer’s disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis.
Compared to currently approved drugs prescribed for the treatment of Alzheimer’s disease, THC is a considerably superior inhibitor of Aβaggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.”
http://www.agoracosmopolitan.com/news/health/2011/11/26/1936.html
A molecular link between the active component of marijuana and Alzheimer’s disease pathology.
“A link between the endocannabinoid system and Alzheimer’s disease has been discovered which has provided a new therapeutic target for the treatment of patients suffering from Alzheimer’s disease. These studies have demonstrated the ability of cannabinoids to provide neuroprotection against β-amyloid peptide (Aβ) toxicity.
Here, we demonstrate that the active component of marijuana, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation, the key pathological marker of Alzheimer’s disease.
Compared to currently approved drugs prescribed for the treatment of Alzheimer’s disease, THC is a considerably superior inhibitor of Aβ aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.
Since the characterization of the Cannabis sativa-produced cannabinoid, Δ9-tetrahydrocannabinol (THC), in the 1960’s,1 this natural product has been widely explored as an anti-emetic, anti-convulsive, anti-inflammatory, and analgesic.”
Read more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562334/
Phosphorylated amyloid-beta: the toxic intermediate in alzheimer’s disease neurodegeneration.
“The results from this study suggest that Abeta phosphorylation could play a role in AD pathology and represent a novel therapeutic target…”