Cannabinoids in Alzheimer’s Disease, Part II


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7/19/2010 2:54 PM RssIcon

You may recall from last week’s installment that some 35 million people worldwide and 5.5 million in the United States have been diagnosed with Alzheimer’s disease, equating to about 5% of people between the ages of 65 and 74 and nearly 50% of people over 85. You may also recall that the numbers appear to be increasing, and that an estimated 10 to 11 million Americans will have been diagnosed with Alzheimer’s disease by 2050.

The cause of the disease is not known. It has been postulated that a combination of genetic, environmental and lifestyle factors may be responsible for the changes in the brain that are associated with Alzheimer’s disease. Although the exact causes of the disease are not well understood, its effects are familiar to millions of people. Early in its course the disease causes difficulty remembering recent events or recently acquired facts, and mild confusion. These symptoms usually worsen over time, with additional symptoms of word-finding difficulty, disorientation, anger, aggression, agitation, loss of appetite and weight loss, depression, or withdrawal becoming increasingly likely. Ultimately, the patient is no longer able to carry out even the simplest tasks of daily living and requires full-time care. The disease also invariably shortens life expectancy, with a median survival of 7 years after diagnosis; only 3% of patients live more than 14 years after the diagnosis is made.

The physical changes in the brain that are responsible for the debilitating deterioration typical of Alzheimer’s disease are characterized by the loss of nerve cells, or neurons, and the connections between them, called synapses, which ultimately leads to atrophy of several areas of the brain. Large areas of plaques, dense deposits of a protein called beta-amyloid, along with tangles of another protein called tau are found in the brains of Alzheimer’s disease patients. These plaques and tangles disrupt vital cellular processes. What sets the deposition of plaques and the development of neurofibrillary tangles in motion isn’t known, though an inflammatory process mediated by substances called “cytokines” that promote inflammation is thought to be an important factor.

There are no effective treatments for Alzheimer’s disease, and although several prescription medications are now available that may reduce the severity of some of the symptoms, they do not alter the ultimate outcome. However, results of a ground-breaking study published in the July 7, 1998 Proceedings of the National Academy of Sciences by Dr. A. J. Hampson et al from the National Institute of Mental Health showed that THC and cannabidiol protected rat neuron cells from damage by glutamate, a neurotransmitter that can injure nerve cells at elevated levels. The authors also found that those substances were more potent antioxidants than vitamin C or vitamin E, and concluded that “The antioxidative properties of cannabinoids suggest a therapeutic use as neuroprotective agents…” They also suggested that they might prevent neurological damage resulting from interruption of blood flow to the brain such as occurs in strokes.

A number of subsequent studies supported their conclusions, and on October 7, 2003 patent number 6630507 was issued to the US Department of Health and Human Services under the title “Cannabinoids as antioxidants and neuroprotectants”.

In the abstract of the patent the authors state that “The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and HIV dementia.”

Please join us again next week as we examine this and other research that supports the potentially major role cannabinoides may play in Alzheimer’s disease and other degenerative neurological conditions.


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