January 05, 2006
Genetic Risk For Alzheimers Causes Brain Insulation Decay
Genetic variations that contribute to risk of Alzheimer's also cause brain nerve insulation to decay.
A new UCLA imaging study shows that age-related breakdown of myelin, the fatty insulation coating the brain's internal wiring, correlates strongly with the presence of a key genetic risk factor for Alzheimer disease.
The findings are detailed in the January edition of the peer-reviewed journal Archives of General Psychiatry and add to a growing body of evidence that myelin breakdown is a key contributor to the onset of Alzheimer disease later in life.
In addition, the study demonstrates how genetic testing coupled with non-invasive evaluation of myelin breakdown through magnetic resonance imaging (MRI) may prove useful in assessing treatments for preventing the disease.
The idea of losing the insulation of the nerves of one's brain with aging strikes me as thoroughly disgusting. We should heavily fund attempts to develop treatments to prevent and reverse brain aging.
A genetic variation in Apolipoprotein E causes the myelin insulating sheaths to break down more rapidly with age.
As the brain continues to develop in adulthood and as myelin is produced in greater and greater quantities, cholesterol levels in the brain increase and eventually promote the production of a toxic protein that attacks the brain. The protein attacks myelin, disrupts message transfer through the axons and eventually can lead to the brain/mind-destroying plaques and tangles visible years later in the cortex of Alzheimer patients.
The Apolipoprotein E (ApoE) genotype is the second most influential Alzheimer risk factor, after only advanced age. The study used MRI to assess myelin breakdown in 104 healthy individuals between ages 55 and 75 and determine whether the shift in the age at onset of Alzheimer disease caused by the ApoE genotype is associated with age-related myelin breakdown.
The results show that in later-myelinating regions of the brain, the severity and rate of myelin breakdown in healthy older individuals is associated with ApoE status. Thus both age, the most important risk factor for Alzheimer disease, and ApoE status, the second-most important risk factor, seem to act through the process of myelin breakdown.
Some people argue that aging is a natural process or a sacred process which we can experience with dignity. But where's the dignity of suffering from a progressive breakdown of the insulation on the nerves of your brain? One doesn't just become gray and wrinkly and move more slowly with age. One's brain goes. One loses the ability to think as well. One is more prone to confusion, less able to deal with the problems of life, less able to recall memories of past events or to remember what one has to accomplish on any given day. There's nothing the least bit dignified about brain decay. It does not bring wisdom. It takes away the ability to recall lessons learned.
Well, would be most interresting how apo AI Milano, the modified version beeing in trials as a medication relates to this finding... would shure be nice to find that the soon available version not only remedies artheriosklerosis but also prevents alzheimer...
am haven't got my answer. the quest is that (what cause brain decay or damaged)and it is true that mastubation and excess sexual conduct causes brain decay,sight effect,weackness of the body.those things are being read and expiriance currently, is there any scientific evidence for that.what type of food or fruit can a person eat to prevent him from brain decay and mental disorder.
Who said Glucosamine could help slow it down??? Read the following Abstract, The more I read, the more I discover that glucosamines interaction in the brain is not neccessarily a good thing for AD. If you want better joints and smooth muscle, perhaps even mylination....take ATP...beware of Glucosamine if you have a chance of AD...You never know.
The role of polysaccharides in the pathogenesis of Alzheimer disease (AD) is unclear. However, in light of studies indicating impaired glucose utilization in AD and increased activation of the hexosamine pathway that is seen with hyperglycemia, in the brains of patients with AD, aberrantly high levels of glucosamine may result in synthesis of glucosamine polymers such as chitin, a highly insoluble polymer of N-acetyl glucosamine, linearized by b1-4 linkages. To examine this further, we studied brain tissue at autopsy from subjects with sporadic and familial AD using calcofluor histochemistry. Calcofluor excites on exposure to ultraviolet light and exhibits a high affinity for chitin in vivo by interacting with b1-4 linkages. Amyloid plaques and blood vessels affected by amyloid angiopathy showed bright fluorescence. Moreover, treatment with chitinase, followed by b-N-acetyl glucosaminidase showed a decrease in calcofluor fluorescence. Since chitin is a highly insoluble molecule and a substrate for glycan-protein interactions, chitin-like polysaccharides within the brain could facilitate nucleation of amyloid proteins in various amyloidoses including AD.
Keywords: alzheimer disease; amyloid; chitin; n-acetyl glucosamine
Document Type: Review article
Affiliations: 1: Department of Pathology, Robert C. Byrd Health Sciences, Center of West Virginia University, P.O. Box 9203, Morgantown, WV 26506-9203, USA.
My wife gave me some of her new diet tofu cookies from Japan that have glucosamine, and I experienced a strange sensation both times I have tried them, so I Googled "Glucosamine effects brain" and here I am. I got a sensation like my skull was expanding and a sense of clarity in my perceptions. I am 42 years old with no history of Alzheimer disease in my family, but I am very sensitive to changes in my body, and these glcosamine cookies definitely have an effect directly on my brain.