Alzheimer’s Disease (AD) is a neurological disorder that is characterized by a loss of memory and learned behavior. Alzheimer’s normally occurs in adults 65 and older and has no cure. The pathology of the disease includes aggregates of the Aβ protein along with the hyperphosphorylation of tau protein, which ultimately leads to the formation of neurofibrillary tangles. These aggregates and tangles cause excitotoxicity and microglial activation, which prompts inflammatory responses, and ultimately lead to cell death.
Cannabis can inhibit the inflammation caused by the abnormal structures formed by Aβ and tau proteins and can also slow the progression of the disease. Investigators at The Scripps Research Institute in California in 2006 reported that THC inhibits the enzyme responsible for the aggregation of amyloid plaques [acetycholinesterase] — the primary marker for Alzheimer's disease — in a manner "considerably superior" to approved Alzheimer's drugs such as donepezil and tacrine. An excerpt from the paper states, "our results provide a mechanism whereby the THC molecule can directly impact Alzheimer's disease pathology. THC and its analogues may provide an improved therapeutic for Alzheimer's disease simultaneously treating both the symptoms and the progression of the disease." (Eubanks, 2006)
This figure from the Scripps Research Institute study shows THC’s effectiveness in reducing the formation of Aβ plaques by inhibiting the enzyme acetylcholinesterase (AChE).
Synthetic cannabinoids have also shown promise in the treatment of AD. Both in vitro and in vivo studies of WIN-55, 212-2 using Aβ treated cells showed a significant decrease in microglia-mediated neurotoxicity (Ramirez, 2005).
A study published in 2007 by V.A. Campbell thoroughly explains the potential of cannabinoids in AD, “The propensity of cannabinoids to reduce β-amyloid-evoked oxidative stress and neurodegeneration, whilst stimulating neurotrophin expression neurogenesis, are interesting properties that may be beneficial in the treatment of Alzheimer's disease. Δ9-tetrahydrocannabinol can also inhibit acetylcholinesterase activity and limit amyloidogenesis, which may improve cholinergic transmission and delay disease progression. Targeting cannabinoid receptors on microglia may reduce the neuroinflammation that is a feature of Alzheimer's disease, without causing psychoactive effects.” (Campbell, 2007)
Newer research has affirmed these positive findings using cannabinoids in mouse models. Researchers from The Roksamp Institute in Sarasota, FL found that the clearance of amyloid beta across the blood brain barrier was doubled in the presence of cannabinoid agonists or inhibitors of the enzymes that degrade cannabinoids (Bachmeier, 2013). This finding is significant because it describes the mechanism of how stimulation of the endocannabinoid system can reduce the burden of Aβ plaques in the brain.
Most recently research published in the journal Neuron from the Stanford School of Medicine has shown that early deficits in Alzheimers such as dementia can be triggered by a loss of the body’s own natural cannabinoids, anandamide and 2-arachidonoylglycerol (2-AG) (Orr, 2014). Based on this research one would think that ingesting exogenous cannabinoids would perform the same role however it would be inaccurate to assume that smoking cannabis could counteract the effects of beta-amyloid plaque on memory and learning “Endocannabinoids in the brain are very transient and act only when important inputs come in,” according to Dr. Daniel Madison, one of the authors of the study. "The primary active ingredient in cannabis, THC, has a much longer lasting effect".
With many significant scientific studies coming out on the therapeutic benefits of the compounds in cannabis there has been a growing interest in understanding how these compounds are produced in the plant. In 2011 these interests resulted in the formation of the company Medicinal Genomics, the first group to sequence the cannabis genome.
Kevin McKernan founder and CEO of Medicinal Genomics states that there are 84 compounds other than THC that could be used to treat a variety of ailments, however anti-drug laws make it difficult for scientists to breed and study the plant in most countries. That’s one of the reasons why he decided to publish the data for free on Amazon’s EC2, a public data cloud. McKernan hopes that their data will help scientists breed cannabis plants with lower THC content and higher amounts of the lesser known cannabinoids.
Check out the Medicinal Genomics website here: www.medicinalgenomics.com
June 22nd and 23rd were two great days for California patients at the High Times Medical Cannabis Cup. The event provided two days of workshops, vendors, music, and of course high grade medicine. Bongs, vapes, joints, pipes, edibles, you name it; it was present at this year’s cup. There were also tons of vendors showing off their newest cannabis innovations and products from Oil Slick pads to “help you concentrate” to the dual grinder container Medtainers. Free dabs were bountiful at this event with the majority of the booths in the 215 areas giving them out like candy. As the sun began to set, Ghostface Killah, Raekwon, and GZA, three members of the notorious Wu-Tang clan took the stage and provided an uplifting performance to a large crowd billowing smoke.
Practice safe dabbing
Bringing science to life at the SC Laboratories booth
Although accompanied by some weather, day two was just as enjoyable with building excitement as the day went on in anticipation of the announcement of the winners of the cup. The evening ended with the presentation of the awards for each category with some of our clients placing!
Congratulations to Santa Cruz Mountain Naturals and SJ Patients Group!
Winners of 1st Place in the Sativa Category and 2nd Place in the Edible Category.
1st Place in the Sativa Category 2nd Place in the Edibles Category
Santa Cruz Mountain Naturals "Cracker Jack" SJ Patients Group "Day Dreamers Medicinal Chocolates"
Recently researchers have discovered that the prevalence of obesity is paradoxically much lower in cannabis users as compared to non-users and that this difference is not accounted for by tobacco smoking status and is still present after adjusting for variables such as sex and age (Le Foll, 2013). In abdominal obesity, the ECS is generally up-regulated in central and peripheral tissues and its blockade results in positive metabolic changes (Silvestri, 2012).
A CB1 antagonist that attempted to harness these positive effects on weight loss was approved by the FDA in February 2006 under the name Rimonabant. However, because CB1 antagonism in the central nervous system causes severe depression and suicidal thoughts the drug was removed from the market shortly after (O'Keefe, 2013).
More recently researchers have focused on developing new CB1 antagonists that can't cross the blood brain barrier restricting them to the periphery. By using compounds that solely target the peripheral ECS, weight loss treatment using this strategy should no longer be accompanied by such negative psychological effects.