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Update November, 2005
One might think that the active ingredients in marijuana
would be more extensively studied in a variety of diseases. Cannabinoids
(active ingredient) seems to have therapeutic effects in amyotrophic lateral
sclerosis (an adult-onset motor neuron disorder), but the researchers
always seem obliged to say things like "However, Delta(9)-tetrahydrocannabinol
(Delta(9)-THC), the predominant cannabinoid in marijuana, induces mind-altering
effects and is partially addictive, compromising its clinical usefulness."
(P. Weydt et at Cannabinol delays symptom onset in SOD1 (G93A)
transgenic mice without affecting survival. Amyotroph Lateral
Scler Other Motor Neuron Disord 2005,
6 (3):182-4.)
A recent article in the Journal of Clinical Investigation
(November, 2005) is an extremely important contribution to the study of
long-term cannabinoid effects. It is entitled "Cannabinoids promote
embryonic and adult hippocampus neurogenesis and produce anxiolytic- and
antidepression-like effects" by Chinese and Canadian researchers
(Wen Jiang et al). Starting with the important fact that (JE Malberg,
2004) that the hippocampus can create new neurons even in adults, the
literature is exploding with information about what promotes neurogenesis
and what happens because of it. This is a complicated field because some
forms of cannabinoids inhibit the neurogenesis in the hippocampus. What
these researchers found was that not only can a synthetic cannabinoid
(HU210) promote neurogenesis but it can do so in a manner consistent with
brain changes related to (we're talking rats) the reduction of anxiety
and depression (the importance of neurogenesis in the hippocampus was
studied earlier in relation to depression). This is counter to the known
supression effects upon such neurogenesis of "all other drugs of
abuse" (alcohol, opiates, nicotine and cocaine). This research is
preliminary and there are indications that even in animal studies researchers
might want to retain a sense of humor (maybe they should consult with
stoners before designing their studies, since the measure of anxiety has
to do with speed of going to a food pellet and eating it in an unfamiliar
cage when food-deprived for 48 hours, after mass cannabinoid use in the
treatment group).
Update: February, 2005
There is some preliminary animal research at the Complutense
University and the Cajal Institute in Madrid reporting that ingredients
in marijuana might stall decline from Alzheimer's disease. These people
are strong researchers: Maria de Ceballos, Journal of Neuroscience.
Earlier Cannabinoid Research: Neuroprotective Effect
Esther Shohami and colleagues at Hebrew University's Medical
Faculty in Jerusalem report that an endogenous cannabinoid plays a role
in the complex protective response prompted by a brain injury. The compound,
2-Arachidonoyl glycerol (2-AG) reportedly occurs in the brain and the
intestine. It can "protect cerebral rat neurons from ischemia in
vitro" , and "synthetic
cannabinoids have been shown to reduce neuronal death in the hippocampus
of rats after experimentally induced ischemia". In this study, the researchers subjected mice
to head trauma and analyzed the 2-AG response following this injury. 2-AG
levels rose, peaking at tenfold after 4 hours. When the researchers injected
additional 2-AG, the mice "developed 50 percent less edema and recovered
faster". More directly relevant to Alzheimer's research, "the
treated mice also suffered less neuronal cell death".
The researchers counted neurons in the CA3 area of the
hippocampus, and report that "control mice (head trauma without exogenous
2-AG) had lost about 40 percent of neurons in that brain area seven days
after the trauma, whereas treated mice lost about 10 percent". (The
hippocampus is among the brain areas most affected by neuronal death in
AD.) The authors write that these results are the first to record the
neuroprotective effects of this cannabinoid. In previous work, the authors
had shown that 2-AG suppresses the formation of reactive oxygen species
and the inflammatory cytokine tumor necrosis factor-alpha, both of which
contribute to the pathophysiology of brain injury. Oxidative damage and
inflammation seem to cause the loss of cells in AD.
October 4, 2001. Nature.
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