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Also check this one out (from Medline: research being done in Spain)

Unique Identifier 15728830

Authors Ramirez BG. Blazquez C. Gomez del Pulgar T. Guzman M. de
Ceballos ML.

Authors Full Name Ramirez, Belen G. Blazquez, Cristina. Gomez del
Pulgar, Teresa. Guzman, Manuel. de Ceballos, Maria L.

Institution Neurodegeneration Group, Cajal Institute, Consejo Superior
de Investigaciones Cientificas, 28002 Madrid, Spain.

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

Source Journal of Neuroscience. 25(8):1904-13, 2005 Feb 23.

Abstract 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.

Publication Type Journal Article.



bearclaw@cruller.invalid wrote:
> http://www.scripps.edu/news/press/080906.html
>
> "According to the new Scripps Research study, which used both computer
> modeling and biochemical assays, THC inhibits the enzyme
> acetylcholinesterase (AChE), which acts as a "molecular chaperone" to
> accelerate the formation of amyloid plaque in the brains of Alzheimer
> victims." [,,,more]