By DRS. DAVID NIESEL AND NORBERT HERZOG
Alzheimer’s disease is the sixth leading cause of U.S. deaths and accounts for up to 80 percent of all dementia cases. Particularly distressing is the fact that there is no way to prevent its occurrence, slow its progression or cure the disease once it is detected. And this produces a significant economic burden on families; totaling almost $250 billion for health care and long term care annually.
More than five million Americans 65 and older are living with Alzheimer’s today, and 16 million are forecast to be afflicted in 2050 at a cost of $1 trillion per year. Yes, one trillion dollars! We have an incomplete understanding of what causes this disease. A protein in the brain called amyloid-beta (Aβ) is thought to play a key role. The Aβ protein aggregates at sites in the brain forming something called plaques. These plaques are not seen in individuals that do not have Alzheimer’s. For some time now, the question has been why do these plaques form?
Recently, there has been an intriguing new possibility regarding the origins of these plaques. It has been proposed that Aβ protein functions to protect the brain from invading microorganisms. Recent experiments reveal that they may be on to something.
Researchers noticed that animals that produce higher levels of Aβ were more resistant to brain infection by exhibiting a longer survival time and lower survival of the bacteria. When tested in the laboratory, Aβ was shown to stick to carbohydrates on the surface of these microbes. Not only that but the Aβ attracted other molecules and extended into fibers that were essential to the antimicrobial activity. Growing fibers entrapped and clumped microbes growing in the laboratory.
Even more intriguing, this ability to clump these microbes occurs during infection in animals. This was demonstrated in the intestinal track after infection with the yeast Candida and administration of Aβ. Other experiments addressed the ability of Aβ to entrap microbes directly in the brain. These experiments used a model that had high levels of Aβ in the mouse brain. A disease causing bacterium was introduced into the mouse brains and what was revealed was fascinating. Within 48 hours, widespread amyloid deposits appeared in the infected brains. When these deposits were analyzed for bacteria, everywhere Aβ deposits were found, there was a bacterium. These results suggest that Aβ deposits may be an important way the brain protects itself from infection. Aβ may be a component of the brain’s innate immune system that is the line of first defenses to control microbial infections. However, in the case of Alzheimer’s, these reactions that defend us can also lead to later problems. Amyloid deposition leads to the neurological damage seen in Alzheimer’s. This could be a game changer.
One could imagine an infection occurring and amyloid deposits being produced years before the symptoms of Alzheimer’s are noticed. This could make the connection between the two events harder to prove and even harder to control. However this could be a smoking gun that could lead to a better understanding of the cause of this heartbreaking disease.
If you would like to join with friends and family from throughout the Bay Area on Oct. 8 for The Walk to End Alzheimer’s, please visit www.alz.org for information and guidance on resources.
Medical Discovery News is a weekly radio and print broadcast highlighting medical and scientific breakthroughs hosted by professor emeritus Norbert Herzog and professor David Niesel, biomedical scientists at the University of Texas Medical Branch at Galveston. Learn more at www.medicaldiscoverynews.com.