Recently an advisory committee to the Food and Drug Administration unanimously recommended the approval of a diagnostic brain scan for Alzheimer’s disease.
The new technology is based upon imaging and quantifying the amount of a specific protein, beta amyloid, in the brains of patients suspected of having the disease. Research has demonstrated a striking correlation between the amount of beta amyloid in the brain and the degree of cognitive impairment in Alzheimer’s patients.
Dr. Norman Foster, professor of neurology at the University of Utah, testified before the FDA committee and was quoted in The New York Times stating the approval of the new scan "would be a historic advance in neurology and in the daily management of patients with memory complaints," an interesting comment as the article goes on to say, "If a person has Alzheimer’s though, there is as yet no treatment that can slow or reverse the disease …"
Over the past several decades, the understanding of beta amyloid’s role as a causative agent for Alzheimer’s disease has served to underpin worldwide research in attempt to develop meaningful treatments designed to rid the brain of this damaging protein. Interestingly, these attempts have met with almost universal failure.
Most recently, pharmaceutical giant Eli Lilly announced yet another failure in an attempt to chemically reduce beta amyloid in humans. In an August 17, 2010 press release the company noted that their experimental drug semagacestat, an "oral agent designed to reduce the body’s production of amyloid beta plaques, which scientists believe play an important role in causing Alzheimer’s disease," actually caused more rapid decline in Alzheimer’s patients. The company revealed that patients treated with the experimental drug "worsened to a significantly greater degree than those treated with placebo."
If beta amyloid were the cause of Alzheimer’s disease, then why would ridding the brain of this protein actually cause patients to worsen?
Harvard researcher Dr. Stephanie Soscia and her associates may have the answer. Their recently published research questioned why beta amyloid accumulates in the Alzheimer’s brain in the first place, and concluded that in fact, the protein actually serves to rid the brain of a variety of bacteria and viruses. They described beta amyloid as an "antimicrobial peptide" which accumulated in response to an infectious agent. Their work looks upon beta amyloid in a new light as they stated, "If the normal function of beta amyloid is to function as an antimicrobial peptide, then an absence of the peptide may result in increased vulnerability to infection."
Rather than causing the disease, beta amyloid may be our brain’s natural response to an infectious agent, accumulating as a way of defending us against a pathogen. So perhaps we should reconsider beta amyloid since it has been said that "the enemy of my enemy is my friend."
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David Perlmutter, M.D., FACN is recognized internationally as a leader in the field of nutritional influences in neurological disorders. A board-certified neurologist, Dr. Perlmutter is the author of bestselling books including Power Up Your Brain: The Neuroscience of Enlightenment and The Better Brain Book .
Dr. Perlmutter has appeared on 20/20, Larry King Live, CNN, Fox News, Fox and Friends , the Today show, The Oprah Show, and The Early Show on CBS. He serves as medical director of the Perlmutter Health Center in Florida and is an adjunct instructor at the Institute for Functional Medicine.
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