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UK: Brain's own cannabis compound protects against inflammation

EurekAlert

Wednesday 04 Jan 2006

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Some clinical studies have indicated that marijuana or its active
cannabinoid ingredient alleviates symptoms of the inflammatory disease
multiple sclerosis (MS). Also, researchers have found that the brain's
natural "endocannabinoids" are released after brain injury and are
believed to alleviate neuronal damage. However, scientists have not
understood how such substances act within the brain's own immune system.

Now, experiments by Oliver Ullrich and colleagues have pinpointed how
one of the brain's endocannabinoids protects neurons from inflammation
after such damage. They say their studies could lead to new drugs to
treat the inflammation and brain degeneration from MS or other such
disorders.

In an article in the January 5, 2006, issue of Neuron, the researchers
reported experiments showing how the endocannabinoid anandamide (AEA)
protects brain cells from inflammation. Such a role in the brain's
immune system is distinct from cannabinoids' effects on neuronal
signaling that produce the behavioral effects of marijuana.

When Ullrich and colleagues analyzed brain tissue from people with MS,
they found elevated levels of AEA, compared to healthy tissue. And in
studies with mouse brain slices, they found that inducing damage with a
brain-cell-exciting chemical, called NMDA, caused an invasion of the
brain's immune cells, called microglia, and an increase in AEA levels.

Importantly, they found that adding AEA to such damaged brain tissue
abolished inflammatory damage to the brain cells, but did not reduce the
primary "excitotoxic" damage from the chemical. They found similar
effects of AEA when they damaged the brain tissue by depriving it of
oxygen and glucose.

The researchers also found that when they used a drug to block the
receptors on microglial cells by which AEA effects the cells,
inflammatory damage was increased.

The researchers also explored the mechanism by which AEA prevents
inflammatory damage. They found that, when AEA plugs into its receptors
on activated microglial cells, it basically activates a specific
molecular signaling pathway that suppresses the production of
inflammation-causing nitric oxide, which would otherwise cause brain injury.

The researchers concluded that the release of AEA in injured brain
tissue might act as a "gatekeeper" and an important "negative-feedback
loop within the CNS [central nervous system] immune system needed to
reduce the extent of the inflammatory response and to limit
neurodegenerative immune reactions after primary brain damage.

"Moreover, endocannabinoid signaling strongly suppresses attack of
microglial cells on nondamaged neurons," they wrote, "suggesting also a
physiological function of the endocannabinoid system in maintaining a
protective and healthy CNS microenvironment."

They also concluded that "the endocannabinoid system represents a local
messenger system between the nervous and immune system and is obviously
involved in the control of immune activation and neuroprotection.
Therefore, elucidating the pathology of the endocannabinoid system
during neuroinflammation and neurodegeneration might open new avenues of
therapeutic interventions in the future."

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The researchers included Eva Eljaschewitsch, Christian Mawrin, Peter M.
Schmidt, Regine Schneider-Stock and Oliver Ullrich of the
Otto-von-Guericke-University Magdeburg in Magdeburg, Germany; Anke
Witting of the University of Washington in Seattle, WA; Thomas Lee,
Heide Hoertnagl and Robert Nitsch of the Charité University Hospital
Berlin in Berlin, Germany; Susanne Wolf of the Max-Delbrueck-Center of
Molecular Medicine in Berlin, Germany; Cedric S. Raine of the Albert
Einstein College of Medicine in New York, NY. This work was supported by
the Research Network N2 of the State Saxony-Anhalt of Germany (O.U.) and
a grant from the Deutsche Forschungsgemeinschaft to R.N., O.U., and
R.S.S. and National Institutes of Health grants (NS 08952 and NS 11920)
to C.S.R.

Eljaschewitsch et al.: "The Endogenous Cannabinoid Anandamide (AEA)
Protects Neurons during CNS Inflammation by Induction of MKP-1 in
Microglial Cells." Publishing in Neuron 49, 67–79, January 5, 2006 DOI
10.1016/j.neuron.2005.11.027 www.neuron.org

 

 

 

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