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Marijuana compound may offer treatment for Alzheimer's disease, study suggests
Posted: Thursday, August 28, 2014 4:45 PM
Joined: 12/6/2011
Posts: 3326

Extremely low levels of the compound in marijuana known as delta-9-tetrahydrocannabinol, or THC, may slow or halt the progression of Alzheimer's disease, a recent study from neuroscientists at the University of South Florida shows. 


Findings from the experiments, using a cellular model of Alzheimer's disease, were reported online in theJournal of Alzheimer's Disease. 


Researchers from the USF Health Byrd Alzheimer's Institute showed that extremely low doses of THC reduce the production of amyloid beta, found in a soluble form in most aging brains, and prevent abnormal accumulation of this protein -- a process considered one of the pathological hallmarks evident early in the memory-robbing disease. These low concentrations of THC also selectively enhanced mitochondrial function, which is needed to help supply energy, transmit signals, and maintain a healthy brain. 


"THC is known to be a potent antioxidant with neuroprotective properties, but this is the first report that the compound directly affects Alzheimer's pathology by decreasing amyloid beta levels, inhibiting its aggregation, and enhancing mitochondrial function," said study lead author Chuanhai Cao, PhD and a neuroscientist at the Byrd Alzheimer's Institute and the USF College of Pharmacy. 


"Decreased levels of amyloid beta means less aggregation, which may protect against the progression of Alzheimer's disease. Since THC is a natural and relatively safe amyloid inhibitor, THC or its analogs may help us develop an effective treatment in the future." 


The researchers point out that at the low doses studied, the therapeutic benefits of THC appear to prevail over the associated risks of THC toxicity and memory impairment. 


Neel Nabar, a study co-author and MD/PhD candidate, recognized the rapidly changing political climate surrounding the debate over medical marijuana. 


"While we are still far from a consensus, this study indicates that THC and THC-related compounds may be of therapeutic value in Alzheimer's disease," Nabar said. "Are we advocating that people use illicit drugs to prevent the disease? No. It's important to keep in mind that just because a drug may be effective doesn't mean it can be safely used by anyone. However, these findings may lead to the development of related compounds that are safe, legal, and useful in the treatment of Alzheimer's disease." 


The body's own system of cannabinoid receptors interacts with naturally-occurring cannabinoid molecules, and these molecules function similarly to the THC isolated from the cannabis (marijuana) plant. 


Dr. Cao's laboratory at the Byrd Alzheimer's Institute is currently investigating the effects of a drug cocktail that includes THC, caffeine as well as other natural compounds in a cellular model of Alzheimer's disease, and will advance to a genetically-engineered mouse model of Alzheimer's shortly. 


"The dose and target population are critically important for any drug, so careful monitoring and control of drug levels in the blood and system are very important for therapeutic use, especially for a compound such as THC," Dr. Cao said. 


  1. Chuanhai Cao et al. The Potential Therapeutic Effects of THC on Alzheimer's Disease. Journal of Alzheimer's Disease, August 2014 DOI: 10.3233/JAD-140093

Posted: Friday, August 29, 2014 12:45 PM
Joined: 9/12/2013
Posts: 3608


 Essentials oils from cannabis for treating dementia and more...



Cannabinoid and Terpene Info

What exactly are the essential oils that we are extracting from the cannabis plant, and what are their properties?


Here is a nifty list that I scored off ICMag, posted by Spurr, who used as his information source:


?-9-tetrahydrocannabinol (THC) Boiling point: 157*C / 314.6 degree Fahrenheit Properties: Euphoriant, Analgesic, Antiinflammatory, Antioxidant, Antiemetic


cannabidiol (CBD) Boiling point: 160-180*C / 320-356 degree Fahrenheit Properties: Anxiolytic, Analgesic, Antipsychotic, Antiinflammatory, Antioxidant, Antispasmodic


Cannabinol (CBN) Boiling point: 185*C / 365 degree Fahrenheit Properties: Oxidation, breakdown, product, Sedative, Antibiotic


cannabichromene (CBC) Boiling point: 220*C / 428 degree Fahrenheit Properties: Antiinflammatory, Antibiotic, Antifungal


cannabigerol (CBG) Boiling point: MP52 Properties:

 Antiinflammatory, Antibiotic, Antifungal

?-8-tetrahydrocannabinol (?-8-THC) Boiling point: 175-178*C / 347-352.4 degree Fahrenheit Properties: Resembles ?-9-THC, Less psychoactive, More stable Antiemetic


tetrahydrocannabivarin (THCV) Boiling point: < 220*C / <428 degree Fahrenheit Properties: Analgesic, Euphoriant


Terpenoid essential oils, their boiling points, and properties

ß-myrcene Boiling point: 166-168*C / 330.8-334.4 degree Fahrenheit Properties: Analgesic. Antiinflammatory, Antibiotic, Antimutagenic

ß-caryophyllene Boiling point: 119*C / 246.2 degree Fahrenheit Properties: Antiinflammatory, Cytoprotective (gastric mucosa), Antimalarial


d-limonene Boiling point: 177*C / 350.6 degree Fahrenheit Properties: Cannabinoid agonist?, Immune potentiator, Antidepressant, Antimutagenic


linalool Boiling point: 198*C / 388.4 degree Fahrenheit Properties: Sedative, Antidepressant, Anxiolytic, Immune potentiator


pulegone Boiling point: 224*C / 435.2 degree Fahrenheit Properties: Memory booster?, AChE inhibitor, Sedative, Antipyretic

1,8-cineole (eucalyptol) Boiling point: 176*C / 348.8 degree Fahrenheit Properties: AChE inhibitor, Increases cerebral, blood flow, Stimulant, Antibiotic, Antiviral, Antiinflammatory,



a-pinene Boiling point: 156*C / 312.8 degree Fahrenheit Properties: Antiinflammatory, Bronchodilator, Stimulant, Antibiotic, Antineoplastic, AChE inhibitor

a-terpineol Boiling point: 217-218*C / 422.6-424.4 degree Fahrenheit Properties: Sedative, Antibiotic, AChE inhibitor, Antioxidant, Antimalarial


terpineol-4-ol Boiling point: 209*C / 408.2 degree Fahrenheit Properties: AChE inhibitor. Antibiotic


p-cymene Boiling point: 177*C / 350.6 degree Fahrenheit Properties: Antibiotic, Anticandidal, AChE inhibitor


Flavonoid and phytosterol components, their boiling points, and properties

apigenin Boiling point: 178*C / 352.4 degree Fahrenheit Properties: Anxiolytic, Antiinflammatory, Estrogenic

quercetin Boiling point: 250*C / 482 degree Fahrenheit Properties: Antioxidant, Antimutagenic, Antiviral, Antineoplastic


cannflavin A Boiling point: 182*C / 359.6 degree Fahrenheit Properties: COX inhibitor, LO inhibitor

ß-sitosterol Boiling point: 134*C / 273.2 degree Fahrenheit Properties: Antiinflammatory, 5-a-reductase, inhibitor

Posted: Tuesday, October 28, 2014 3:21 PM
Joined: 9/12/2013
Posts: 3608


Posted: Tuesday, October 28, 2014 3:22 PM
Joined: 9/12/2013
Posts: 3608

VIDEO on cannabis science

Lane Simonian
Posted: Saturday, November 1, 2014 12:09 PM
Joined: 12/12/2011
Posts: 4986

An interesting study on the anti-anxiety anti-psychotic effects of cannabidiol with implications for the treatment of neuropsychiatric problems in Alzheimer's disease. 


Marijuana Compound May Beat Antipsychotics at Treating Schizophrenia

By  Associate News Editor
Reviewed by John M. Grohol, Psy.D. on June 7, 2012 

Marijuana Compound May Beat Antipsychotics at Treating SchizophreniaA certain marijuana compound known as cannabidiol (CBD) can treat schizophrenia as well asantipsychotic drugs, with far fewer side effects, according to a preliminary clinical trial.


The research team, led by Markus Leweke of the University of Cologne in Germany, studied 39 people with schizophrenia who were hospitalized for a psychotic episode. Nineteen patients were treated with amisulpride, an antipsychotic medication that is not approved in the U.S., but is similar to other approved drugs.


The remaining 20 patients were given CBD, a substance found in marijuana that is considered responsible for the mellowing oranxiety-reducing effects. Unlike the main ingredient in marijuana, THC, which can trigger psychotic episodes and worsen schizophrenia, CBD has antipsychotic effects, according to prior research in both animals and humans.


Neither the patients nor the scientists knew who was receiving which drug. At the end of the four-week trial, both groups made significant clinical improvements in their schizophrenic symptoms, and there was no difference between those getting CBD or amisulpride.


“The results were amazing,” said Daniel Piomelli, Ph.D., professor of pharmacology at the University of California-Irvine and a co-author of the study. “Not only was [CBD] as effective as standard antipsychotics, but it was also essentially free of the typical side effects seen with antipsychotic drugs.”


Antipsychotic drugs may cause devastating and sometimes permanent movement disorders; they can also lower a patient’s motivation and pleasure. The new generation of these drugs can also lead to weight gain and increase the risk for diabetes. These side effects are well known as a major hindrance during treatment.


In the German study, weight gain and movement problems were observed in patients taking amisulpride, but not CBD.


“These exciting findings should stimulate a great deal of research,” said Dr. John Krystal, chair of psychiatry at Yale University School of Medicine, who was not associated with the research. He notes that CBD not only had fewer side effects, but also seemed to work better on schizophrenia’s so-called “negative symptoms,” which are notoriously hard to treat.


Negative symptoms of schizophrenia include social withdrawal, a lowered sense of pleasure and a lack of motivation. However, since current antipsychotic medications can actually cause these negative symptoms, it wasn’t clear whether CBD was better than amisulpride at getting rid of these symptoms, or whether CBD simply caused fewer side effects to begin with.


If replicated, the results suggest that CBD may be at least as effective as current medications for the treatment of schizophrenia, without the severe side effects that make patients reluctant to take medication.


“The real problem with CBD is that it’s hard to develop for a variety of silly reasons,” said Piomelli. Since it comes from marijuana, there are obvious political issues surrounding its use. Extracting it from the plant is also expensive.


But the biggest obstacle may be that CBD is a natural compound, and therefore can’t be patented the way new drugs are. So although CBD could outsell the current blockbuster antipsychotic drugs, pharmaceutical companies aren’t likely to develop it. Researchers are working to develop synthetic versions of CBD that would avoid such hurdles.


“We have one and are hoping to move forward in the near future,” Piomelli said.


The study is published online in the journal Translational Psychiatry. 



Posted: Tuesday, November 4, 2014 10:51 AM
Joined: 9/12/2013
Posts: 3608

Quote (Regarding use of cannabinoids and ALZ)

Conclusions and therapeutic implications


Considering the numerous complex pathological mechanisms involved in the
progression of AD, treatments targeting a single causal or modifying factor offer limited
benefit. Cannabinoids, however, exhibit pleiotropic activity, targeting in parallel several
processes that play key roles in AD, including Aβ and tau aberrant processing,
neuroinflammation, excitotoxicity, mitochondrial dysfunction, and oxidative stress.
Cannabinoids improve behavioral disturbances, as well. These effects are summarized
in Figure 1. Then, because of these widespread properties of cannabinoid compounds,
targeting the ECS could represent a unique and reliable opportunity to advance towards
an effective therapy against the AD. Moreover, cannabinoids might represent a safe
low-cost therapy, with their natural origin and low side effects profile. From our point
of view, the success of cannabinoid-based therapy in AD could be increased taking into
account two important aspects: (i) the use of a combination of compounds that cover the
whole spectrum of therapeutic properties described for cannabinoids, i.e. combination
of CB1 and CB2 receptors agonists plus CBD, which presents interesting
neuroprotective properties spite of its mechanism of action remaining poorly
understood, and (ii) the early initiation of the treatment in the neurodegenerative
process, which ensures the integrity of the ECS target components and increases the
possibility of curbing the exponential degenerative progression toward dementia.


http://www.frontiers...isional PDF.pdf

Lane Simonian
Posted: Tuesday, November 4, 2014 3:42 PM
Joined: 12/12/2011
Posts: 4986

This really is it: compounds from marijuana and other aromatic plants inhibit the formation of amyloid (which ironically is the least important thing that they do) and aberrant tau processing, reduce oxidative stress, lessen neuroinflammation, lower excitoxicity and protect the mitochondria (which helps protect against the death of neurons), and in most cases improve mood and behavior in people with Alzheimer's disease.  It is likely that if you combine these aromatic plants (medicinal marijuana, aromatherapy using various essential oils, lemon balm extract, hops, Angelica archangelica, and panax ginseng, for instance), the results are even better.  

There is not much more to do except to spread the message that Alzheimer's disease is not a death sentence.  The disease can be kept in check with certain antioxidants found in various plants.  To a certain extent it can be reversed even in the very latest stages.  

Lane Simonian
Posted: Wednesday, November 5, 2014 4:29 PM
Joined: 12/12/2011
Posts: 4986

Another valuable article on the use of cannabinoids in marijuana to treat Alzheimer's disease. 


 2005 Feb 23;25(:1904-13.

Prevention of Alzheimer's disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation.


Alzheimer's disease (AD) is characterized by enhanced beta-amyloid peptide (betaA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo. This background prompted us to study the localization, expression, and function of cannabinoid receptors in AD and the possible protective role of cannabinoids after betaA treatment, both in vivo and in vitro. Here, we show that senile plaques in AD patients express cannabinoid receptors CB1 and CB2, together with markers of microglial activation, and that CB1-positive neurons, present in high numbers in control cases, are greatly reduced in areas of microglial activation. In pharmacological experiments, we found that G-protein coupling and CB1 receptor protein expression are markedly decreased in AD brains. Additionally, in AD brains, protein nitration is increased, and, more specifically, CB1 and CB2 proteins show enhanced nitration. Intracerebroventricular administration of the synthetic cannabinoid WIN55,212-2 to rats prevent betaA-induced microglial activation, cognitive impairment, and loss of neuronal markers. Cannabinoids (HU-210, WIN55,212-2, and JWH-133) block betaA-induced activation of cultured microglial cells, as judged by mitochondrial activity, cell morphology, and tumor necrosis factor-alpha release; these effects are independent of the antioxidant action of cannabinoid compounds and are also exerted by a CB2-selective agonist. Moreover, cannabinoids abrogate microglia-mediated neurotoxicity after betaA addition to rat cortical cocultures. Our results indicate that cannabinoid receptors are important in the pathology of AD and that cannabinoids succeed in preventing the neurodegenerative process occurring in the disease.


However, it has everything to do with the antioxidant effects of cannabinoids and particularly their ability to partially reverse the oxidation and nitration caused by peroxynitrites. 


 2003 Nov;163(5):1997-2008.

Neuroprotective effect of (-)Delta9-tetrahydrocannabinol and cannabidiol in N-methyl-D-aspartate-induced retinal neurotoxicity: involvement of peroxynitrite.


In glaucoma, the increased release of glutamate is the major cause of retinal ganglion cell death [excitoxicity]. Cannabinoids have been demonstrated to protect neuron cultures from glutamate-induced death. In this study, we test the hypothesis that glutamate causes apoptosis of retinal neurons via the excessive formation of peroxynitrite, and that the neuroprotective effect of the psychotropic Delta9-tetrahydroxycannabinol (THC) or nonpsychotropic cannabidiol (CBD) is via the attenuation of this formation. Excitotoxicity of the retina was induced by intravitreal injection of N-methyl-D-aspartate (NMDA) in rats, which also received 4-hydroxy-2,2,6,6-tetramethylpiperidine-n-oxyl (TEMPOL,a superoxide dismutase-mimetic), N-omega-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase inhibitor), THC, or CBD. Retinal neuron loss was determined by TDT-mediated dUTP nick-end labeling assay, inner retinal thickness, and quantification of the mRNAs of ganglion cell markers. NMDA induced a dose- and time-dependent accumulation of nitrite/nitrate, lipid peroxidation, and nitrotyrosine (foot print of peroxynitrite), and a dose-dependent apoptosis and loss of inner retinal neurons. Treatment with L-NAME or TEMPOL protected retinal neurons and confirmed the involvement of peroxynitrite in retinal neurotoxicity. The neuroprotection by THC and CBD was because of attenuation of peroxynitrite. The effect of THC was in part mediated by the cannabinoid receptor CB1. These results suggest the potential use of CBD as a novel topical therapy for the treatment of glaucoma.


And to drive the point home with another aromatic compound: 


 2007 Jun 18;180(2):139-45. Epub 2007 Mar 12.

A natural scavenger of peroxynitrites, rosmarinic acid, protects against impairment of memory induced by Abeta(25-35).


Peroxynitrite (ONOO(-))-mediated damage is regarded to be responsible for the cognitive dysfunction induced by amyloid beta protein (Abeta) in Alzheimer's disease (AD). In the present study, we examined the protective effects of rosmarinic acid (RA), a natural scavenger of ONOO(-), on the memory impairment in a mouse model induced by acute i.c.v. injection of Abeta(25-35). Mice daily received i.p. several doses of RA after the injection of Abeta(25-35). RA prevented the memory impairments induced by Abeta(25-35) in the Y maze test and novel object recognition task. RA, at the effective lowest dose (0.25mg/kg), prevented Abeta(25-35)-induced nitration of proteins, an indirect indicator of ONOO(-) damage, in the hippocampus. At this dose, RA also prevented nitration of proteins and impairment of recognition memory induced by ONOO(-)-i.c.v.-injection. Co-injection of the non-memory-impairing dose of ONOO(-) with Abeta(25-35) blocked the protective effects of RA (0.25mg/kg). These results demonstrated that the memory protective effects of RA in the neurotoxicity of Abeta(25-35) is due to its scavenging of ONOO(-), and that daily consumption of RA may protect against memory impairments observed in AD.


I have contacted a university lab in North Carolina studying the effects of different natural compounds for their abilities to scavenge peroxynitrites and treat neurodegenerative disease.  They just need to keep screening phenolic compounds until they find the ones that work the best. 


In the meantime, find the combination of phenolic compounds in herbs and essential oils that work best for you or for your loved one--noting any side effects and adjusting doses as needed. It is not optimal, but being proactive is the best option until the scientists, policy makers, and administrators with the power to change the course of this disease catch up or catch on.  



Lane Simonian
Posted: Thursday, November 6, 2014 11:55 AM
Joined: 12/12/2011
Posts: 4986

I wrote to the lead scientist-Chuanhai Cai--on the THC study and to my surprise he wrote back right away and said that he would keep me informed of further results using THC, caffeine, and other natural compounds to treat Alzheimer's disease.  He is doing invaluable research and seems like a very nice man.  I will pass along any new information that I receive.
Posted: Sunday, November 23, 2014 1:14 AM
Joined: 10/8/2014
Posts: 469

This is great. I was doing research on medical marijuana for my grandma. Unfortunately her state doesn't have laws regarding using it for medicinal purposes. There is currently a drig available that is a synthetic Delta 9 THC called Marinol. I am going to have to put more tim  into this thread & print it oit for her nuero to see about getting her on it.