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Helping Glial Cells will Revolutionize Prevention & Treatment of Alzheimer's
October 1, 2009
In the face of a baby boomer population certain to have an epidemic of cognitive decline and Alzheimer's there is very good news on the cutting edge of science for those interested in being proactive on the topic. The rapid developments in our understanding of neurobiology are causing scientists to refocus their efforts on the healthy function of glial cells in order to maintain and restore cognitive health.
Much of Alzheimer's research focuses on amyloid beta peptide that is obviously involved in the plaque tangles in the brain of those with cognitive decline and Alzheimer's. However, targeting the reduction of this protein has minimal value in terms of a therapeutic response. That is because the accumulation of amyloid plaque is the end result of a process of poor brain health, not the cause of the problem in and of itself. A similar example is that of cholesterol lining the arteries in the form of plaque. It is not the cholesterol itself that is the problem; it is the process that leads to plaque formation in the arteries.
A more expanded view of neurologic health has been coined the “myelin model.” Its major proponent is UCLA professor of psychiatry George Bartzokis, and his theory which has been evolving for years was just published in the Neurobiology of Aging1. There is much to be said for what Dr. Bartzokis has to say.
Like insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functions and encoding of memories.
But the lifelong, extensive myelination of the human brain also makes it uniquely vulnerable to damage. The myelin model's central premise is that it is the normal, routine maintenance and repair of myelin throughout life that ultimately initiates the mechanisms that produce degenerative diseases like Alzheimer's. That is, the amyloid-beta peptide and the tau peptide, which is also implicated in Alzheimer's, as well as the signature clinical signs of the disease, such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown and repair processes.
“The pervasive myelination of our brain is the single most unique aspect in which the human brain differs from other species,” said Bartzokis.
Myelin is produced by specialized glial cells called oligodendrocytes. The healthy function of these cells begins to decline in our 50s, resulting in more amyloid beta plaque formation due to the poor function of these cells trying to cope with the process of aging. These glial cells are sensitive to inflammation damage and consequent excess free radical production, in turn leading to neurologic malfunction that could readily be behind virtually all age-associated nerve problems.
Glial cells are the new frontier for maintaining intelligence, cognitive function, mood, memory, and the ability to learn. While much of this information is relevant to diseases of deterioration, it is equally important to maximizing genetic potential and can be used to support the development of optimal intelligence.
Much of Alzheimer's research focuses on amyloid beta peptide that is obviously involved in the plaque tangles in the brain of those with cognitive decline and Alzheimer's. However, targeting the reduction of this protein has minimal value in terms of a therapeutic response. That is because the accumulation of amyloid plaque is the end result of a process of poor brain health, not the cause of the problem in and of itself. A similar example is that of cholesterol lining the arteries in the form of plaque. It is not the cholesterol itself that is the problem; it is the process that leads to plaque formation in the arteries.
A more expanded view of neurologic health has been coined the “myelin model.” Its major proponent is UCLA professor of psychiatry George Bartzokis, and his theory which has been evolving for years was just published in the Neurobiology of Aging1. There is much to be said for what Dr. Bartzokis has to say.
Like insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functions and encoding of memories.
But the lifelong, extensive myelination of the human brain also makes it uniquely vulnerable to damage. The myelin model's central premise is that it is the normal, routine maintenance and repair of myelin throughout life that ultimately initiates the mechanisms that produce degenerative diseases like Alzheimer's. That is, the amyloid-beta peptide and the tau peptide, which is also implicated in Alzheimer's, as well as the signature clinical signs of the disease, such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown and repair processes.
“The pervasive myelination of our brain is the single most unique aspect in which the human brain differs from other species,” said Bartzokis.
Myelin is produced by specialized glial cells called oligodendrocytes. The healthy function of these cells begins to decline in our 50s, resulting in more amyloid beta plaque formation due to the poor function of these cells trying to cope with the process of aging. These glial cells are sensitive to inflammation damage and consequent excess free radical production, in turn leading to neurologic malfunction that could readily be behind virtually all age-associated nerve problems.
Glial cells are the new frontier for maintaining intelligence, cognitive function, mood, memory, and the ability to learn. While much of this information is relevant to diseases of deterioration, it is equally important to maximizing genetic potential and can be used to support the development of optimal intelligence.
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