You may have heard that amyloid plaques and neurofibrillary tangles contribute to the development of Alzheimer's disease (AD). Do you know what these plaques and tangles are? And what do we really know about where they fit in the Alzheimer's puzzle?
Amyloids are protein fragments that everyone has. Their production is a normal thing for all of us. Beta amyloids are protein fragments from something called an amyloid precursor protein, or APP. Again, the presence of beta amyloids is a normal state of affairs.
Things seem to start to fall apart when these fragments don't get broken down and eliminated by the body. When the fragments continue to gather, forming hard amyloid plaques, the potential for Alzheimer's disease emerges.
Neurofibrillary tangles are twisted fibers in cells of the brain. They're mostly made from tau, which is a protein. Tau is a component of a microtubule. Under normal circumstances, nutrients and other vital materials are sent via tubules from one area of a nerve cell to another.
If the tau protein has some abnormality, the microtubules can't sustain themselves, and they collapse.
The underlying belief amongst researchers and the medical community has been that amyloid plaques and tangles are causative factors for AD. But an article from July 26, 2010 on the LA Times website pointed to research that suggests otherwise.
Maria Carrillo, director of medical and scientific relations at the Alzheimer's Association said, "Perhaps those are just byproducts of some other pathology that is really the more important key. We really don't know all that yet."
Carrillo paints this picture. As early as 10 to 15 years before AD shows itself, beta amyloid begins to change. Abnormal amyloid begins to affect tau protein, and tangles ensue. The tangles are credited with holes in the memory which begin to occur.
Eventually the brain is overcome by amyloid plaques and tau tangles, becoming less able to function effectively. Neurons (nerve cells) are dying. The brain is in disarray.
Did the plaques and tangles cause this destruction, or are they simply by-products of some other dynamic?
Another assumption being re-examined is that the problem originates in the brain. But according to an article from March 4, 2011 on Evoscience.com, research from a Scripps Research Institute and ModGene, LLC study is raising questions.
Findings seemed to indicate that the buildup of beta amyloid may actually begin in the liver, being delivered to the brain via the bloodstream. Researchers speculate that if this is indeed the case, Alzheimer's may be prevented by hindering beta amyloid production in the liver.
Certainly more research is in order. Nevertheless, Greg Sutcliffe, Scripps Research Professor and leader of the study, believes that the new data "holds promise for the development of new therapies to fight Alzheimer’s.”
Plaques and Tangles. Ahaf.org. September 26, 2011. Retrieved October 12, 2011.
Studies target amyloid plaques and tau tangles. Articles.latimes.com. July 26, 2010. Retrieved October 12, 2011.
Liver, Not Brain, May Be Origin of Alzheimer's Plaques. Evoscience.com. Retrieved October 12, 2011.
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Reviewed October 13, 2011
by Michele Blacksberg RN