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cannabinoids can reduce pathological processes associated with Alzheimer's disease
![[Image: genetics_AD.png]](http://www.cnsforum.com/content/pictures/imagebank/hirespng/genetics_AD.png)
Research by scientists of Madrid's Complutense University and the Cajal Institute published in the Journal of Neuroscience has demonstrated that cannabinoids can reduce pathological processes associated with Alzheimer's disease. Researchers hope that cannabinoids may be used to develop new drug therapies against the disease.
They first compared the brain tissue of patients who died from Alzheimer's disease with that of healthy people who had died at a similar age. The researchers found a dramatically reduced functioning of cannabinoid receptors in diseased brain tissue and markers of microglia activation. Microglia activate the brain's immune response and are found near the plaque deposits associated with Alzheimer's disease. When active, microglia cause inflammation. Nerve cells with cannabinoid-1 receptors (CB1), present in high numbers in control subjects, were greatly reduced in areas of microglial activation.
In a second step rats were injected with amyloid-beta peptide. This protein plays an important role in Alzheimer's disease, since increased brain levels of amyloid-beta are supposed to result in aggregation of this protein to form plaques. Animals who also received different cannabinoids performed better in tests of their mental functioning. Analyses showed that cannabinoids had prevented microglial activation and thus had reduced inflammation. These effects were also mediated by cannabinoids that only bind to CB2 receptors.
Researchers concluded: "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."
British researchers, who published their work in the journal Sub-Cellular Biochemistry, found that phosphorylation of amyloid-beta increased the neurotoxicity of this protein. And they demonstrated that cannabinoids prevented these damaging effects of phosphorylated amyloid-beta on nerve cells.
(Sources: Ramirez BG, et al. Prevention of Alzheimer's disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation. J Neurosci 2005;25(8):1904-13; Milton NG. Phosphorylated amyloid-beta: the toxic intermediate in alzheimer's disease neurodegeneration. Subcell Biochem 2005;38:381-402; BBC News of 22 February 2005)
more
Research by scientists of Madrid's Complutense University and the Cajal Institute published in the Journal of Neuroscience has demonstrated that cannabinoids can reduce pathological processes associated with Alzheimer's disease. Researchers hope that cannabinoids may be used to develop new drug therapies against the disease.
They first compared the brain tissue of patients who died from Alzheimer's disease with that of healthy people who had died at a similar age. The researchers found a dramatically reduced functioning of cannabinoid receptors in diseased brain tissue and markers of microglia activation. Microglia activate the brain's immune response and are found near the plaque deposits associated with Alzheimer's disease. When active, microglia cause inflammation. Nerve cells with cannabinoid-1 receptors (CB1), present in high numbers in control subjects, were greatly reduced in areas of microglial activation.
In a second step rats were injected with amyloid-beta peptide. This protein plays an important role in Alzheimer's disease, since increased brain levels of amyloid-beta are supposed to result in aggregation of this protein to form plaques. Animals who also received different cannabinoids performed better in tests of their mental functioning. Analyses showed that cannabinoids had prevented microglial activation and thus had reduced inflammation. These effects were also mediated by cannabinoids that only bind to CB2 receptors.
Researchers concluded: "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."
British researchers, who published their work in the journal Sub-Cellular Biochemistry, found that phosphorylation of amyloid-beta increased the neurotoxicity of this protein. And they demonstrated that cannabinoids prevented these damaging effects of phosphorylated amyloid-beta on nerve cells.
(Sources: Ramirez BG, et al. Prevention of Alzheimer's disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation. J Neurosci 2005;25(8):1904-13; Milton NG. Phosphorylated amyloid-beta: the toxic intermediate in alzheimer's disease neurodegeneration. Subcell Biochem 2005;38:381-402; BBC News of 22 February 2005)
more