[extropy-chat] Cannabis vs Alzheimer's

[Ian Goddard]

Given the anticholinergic property of THC one might
not imagine cannabis would be a potential source of
anti-Alzheimer's therapeutics (its anticholinergic
effect probably underlies the impression that cannabis
makes its users stupid); but given the emerging data
that cannabionoids (including THC) are
neuroprotective, these data are not too shocking:


http://www.jneurosci.org/cgi/content/abstract/25/8/1904

The Journal of Neuroscience, February 23, 2005.

Prevention of Alzheimer's Disease Pathology by
Cannabinoids: Neuroprotection Mediated by Blockade of
Microglial Activation 

[authors and affiliations cut for brevity, see link]

Alzheimer's disease (AD) is characterized by enhanced
[beta]-amyloid peptide ([beta]A) 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 [beta]A
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
[beta]A-induced microglial activation, cognitive
impairment, and loss of neuronal markers. Cannabinoids
(HU-210, WIN55,212-2, and JWH-133) block
[beta]A-induced activation of cultured microglial
cells, as judged by mitochondrial activity, cell
morphology, and tumor necrosis factor- 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 [beta]A
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. 

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Pop press report on the same study: 

Marijuana may block Alzheimer's 
http://news.bbc.co.uk/1/hi/health/4286435.stm

****************************************************

Previous related studies:

J Neurochem 2004: Neuroprotective effect of
cannabidiol, a non-psychoactive component from
Cannabis sativa, on beta-amyloid-induced toxicity in
PC12 cells. PubMed ID: 15030397
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15030397


Neurosci Lett 2002: Anandamide and noladin ether
prevent neurotoxicity of the human amyloid-beta
peptide. PubMed ID: 12384227 
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12384227

See also:
http://www.mapinc.org/drugnews/v02/n1817/a02.html?107


http://iangoddard.net

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