First some background:
Cancer refers to the uncontrolled growth of cells within the human body. This uncontrolled growth leads to what is known as tumors, of which there are two types, benign and malignant. While benign tumors pose no serious threat, malignant tumors are capable of invading and eventually destroying nearby tissue as well as what is known as metastasis, which is the spread of cancer cells to other parts of the body. In breast cancer cells, the receptors for cannabinoids tend to be overexpressed compared to normal breast tissue
The new information:
When the cannabinoid receptors on breast cancer cells are activated, cell growth, division, and migration were inhibited. In this specific experiment, mouse breast cancer models showed a 40-50% reduction in tumor growth and a 65-80% reduction in lung metastasis (spread of cancer to the lungs). Also, in PyMT mouse models, which are analogous to human invasive ductal carcinoma, cannabinoid receptor activation led to a reduction in tumor size and not just growth. This reduction was shown to be the result of programmed cell death, or apoptosis, which the cannabinoids induced.
What this means:
This research shows that cannabinoids could potentially be used to protect against the growth and spread of breast cancer.
Qamri, Z, et al. “Synthetic cannabinoid receptor agonists inhibit tumor growth and metastasis of breast cancer.” Molecular cancer therapeutics. 8.11 (2009): 3117-29.
Friday, January 29, 2010
December 2009: Cannabinoid receptor-1 activation in the spinal cord leads to an inhibition of nerve cell damage and death. (Cleveland Clinic, Clevelan
First some background:
in conditions known as neurodegenerative diseases, such as Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and Lou Gehrig’s disease (ALS, amylotrophic lateral sclerosis), one of the major problems is what is
referred to as excitotoxicity. Excitotoxicity is when cells in our brain are overexcited by natural signals, leading to cell damage and eventually death. A well-known mechanism for the development of the aforementioned neurodegenerative diseases is the excitotoxicity of glutamate receptors on brain cells (glutamate is one of our body’s natural signals). These glutamate receptors have two main subtypes, NMDA and AMPA, with their names referring to an artificial substance that can perform the same role as the natural signal, glutamate.
The new information:
Within the spinal cord, nerve cells that send signals to the brain can be prevented from damage and death due to excitotoxicity. Within these nerve cells, excitotoxicity is mediated through NMDA glutamate receptors. This new research involved exposing the spinal cord nerve cells to NMDA (N-methyl-D-aspartic acid) in the presence of cannabinoids. It was found that the toxic effects of NMDA (and therefore the natural signal, glutamate) were blocked when the cannabinoids were present.
What this means:
This research simply provides more evidence for what is already generally known, that cannabinoids can slow down and even potentially stop the progression of neurodegenerative diseases. Bhat, M, WD Bowen, J Cheng, and Q Liu.
“Signaling pathways from cannabinoid receptor-1 activation to inhibition of N-methyl-D-aspartic acid mediated calcium influx and neurotoxicity in dorsal root ganglion neurons.” The Journal of pharmacology and experimental therapeutics. 331.3 (2009): 1062-70.
in conditions known as neurodegenerative diseases, such as Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and Lou Gehrig’s disease (ALS, amylotrophic lateral sclerosis), one of the major problems is what is
referred to as excitotoxicity. Excitotoxicity is when cells in our brain are overexcited by natural signals, leading to cell damage and eventually death. A well-known mechanism for the development of the aforementioned neurodegenerative diseases is the excitotoxicity of glutamate receptors on brain cells (glutamate is one of our body’s natural signals). These glutamate receptors have two main subtypes, NMDA and AMPA, with their names referring to an artificial substance that can perform the same role as the natural signal, glutamate.
The new information:
Within the spinal cord, nerve cells that send signals to the brain can be prevented from damage and death due to excitotoxicity. Within these nerve cells, excitotoxicity is mediated through NMDA glutamate receptors. This new research involved exposing the spinal cord nerve cells to NMDA (N-methyl-D-aspartic acid) in the presence of cannabinoids. It was found that the toxic effects of NMDA (and therefore the natural signal, glutamate) were blocked when the cannabinoids were present.
What this means:
This research simply provides more evidence for what is already generally known, that cannabinoids can slow down and even potentially stop the progression of neurodegenerative diseases. Bhat, M, WD Bowen, J Cheng, and Q Liu.
“Signaling pathways from cannabinoid receptor-1 activation to inhibition of N-methyl-D-aspartic acid mediated calcium influx and neurotoxicity in dorsal root ganglion neurons.” The Journal of pharmacology and experimental therapeutics. 331.3 (2009): 1062-70.
January 2010: Cannabinoids prevent and may aid in healing cell damage in multiple sclerosis. (Instituto Cajal, Madrid, Spain)
Cannabinoids prevent and may aid in healing cell damage in multiple sclerosis. (Instituto Cajal, Madrid, Spain)
First some background:
Multiple sclerosis is caused by cell damage in the brain and spinal cord, leading to a decreased ability of the body to communicate effectively with itself. One of the possible causes of multiple sclerosis is excitotoxicity mediated by AMPA glutamate receptors (see December 2009), but the root cause is the gradual damage and loss of the fatty myelin sheath surrounding specific areas of nerve cells. The myelin sheath is basically a layer of insulation which allows fast and precise electrical communication between cells within the brain and spinal cord.
The new information:
In mouse models of TMEV-IDD (Theiler’s murine encephalomyelitis virus-induced demyelinating disease) multiple sclerosis, increased cannabinoid levels led to protection against excitotoxicity, and thus protection against cell damage. In the experiment performed, an uptake blocker was introduced in order to increase the levels of cannabinoids at the junction between two cells. The increased level of cannabinoids led not only to the inhibition of excitotoxicity, but also activation of a factor within the cells which causes genetic changes. This factor is known as PPAR-gamma (peroxisome proliferator-activated receptor gamma), and it causes our DNA to tell the cell to produce more fat (recall that multiple sclerosis is caused by the destruction of the fatty insulation surrounding part of the nerve cell).
What this means:
Not only did this research provide more evidence that cannabinoids protect against neurodegenerative diseases, but that they may also aid in healing the cause of multiple sclerosis at a molecular level.
Loria, F, et al. “An endocannabinoid tone limits excitotoxicity in vitro and in a model of multiple sclerosis.” Neurobiology of disease. 37.1 (2010): 166-76.
First some background:
Multiple sclerosis is caused by cell damage in the brain and spinal cord, leading to a decreased ability of the body to communicate effectively with itself. One of the possible causes of multiple sclerosis is excitotoxicity mediated by AMPA glutamate receptors (see December 2009), but the root cause is the gradual damage and loss of the fatty myelin sheath surrounding specific areas of nerve cells. The myelin sheath is basically a layer of insulation which allows fast and precise electrical communication between cells within the brain and spinal cord.
The new information:
In mouse models of TMEV-IDD (Theiler’s murine encephalomyelitis virus-induced demyelinating disease) multiple sclerosis, increased cannabinoid levels led to protection against excitotoxicity, and thus protection against cell damage. In the experiment performed, an uptake blocker was introduced in order to increase the levels of cannabinoids at the junction between two cells. The increased level of cannabinoids led not only to the inhibition of excitotoxicity, but also activation of a factor within the cells which causes genetic changes. This factor is known as PPAR-gamma (peroxisome proliferator-activated receptor gamma), and it causes our DNA to tell the cell to produce more fat (recall that multiple sclerosis is caused by the destruction of the fatty insulation surrounding part of the nerve cell).
What this means:
Not only did this research provide more evidence that cannabinoids protect against neurodegenerative diseases, but that they may also aid in healing the cause of multiple sclerosis at a molecular level.
Loria, F, et al. “An endocannabinoid tone limits excitotoxicity in vitro and in a model of multiple sclerosis.” Neurobiology of disease. 37.1 (2010): 166-76.
Sunday, January 24, 2010
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