We should reconsider our thought process on what underlies Alzheimer's, especially as it relates to the role of beta-amyloid. Remember, the enemy of my enemy is my friend.
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Alzheimer's now affects more than 5.4 million Americans and may be costing as much as $200 billion annually, twice what is spent on cardiovascular disease and close to triple what is spent on treating cancer, according to a recent RAND study.

The central thesis in terms of what causes Alzheimer's, has focused on the role of a particular protein, beta-amyloid, as a cornerstone in the degeneration of the brain seen in this disease. In fact, new brain-imaging technology is now available that can actually determine the amount of this protein in people as a way to help predict their Alzheimer's risk. But in the absence of any meaningful treatment, the utility of this line of investigation is questionable. I'll leave that be, but indicate that clearly half of individuals studied who are found to have significant elevations of beta-amyloid are completely intact from a cognitive perspective.

Focusing on the purported role of beta-amyloid in Alzheimer's has led to pharmaceutical researchers expending incredible resources to find drugs to rid the brain of this seemingly dreadful protein. And thus far, all efforts have failed, miserably.

It comes as no surprise that a study published recently in the New England Journal of Medicine is yet another report of the failure of a drug, one designed to reduce beta-amyloid in the brains of people at risk for Alzheimer's disease, has not only failed, but its use, compared to placebo, actually led to worsening of cognitive function. This finding should cause researchers and clinicians alike to question their perception of beta-amyloid. If reducing amyloid in the brain makes people decline more rapidly, perhaps it isn't the problem. Perhaps it is actually doing the brain good.

It turns out that beta-amyloid is an "antimicrobial peptide," a technical term for a protein that helps get rid of foreign organisms. Indeed, Dr. Ruth Itzhaki from the University of Manchester has published extensively demonstrating compelling evidence of the central role of the herpes simplex virus in Alzheimer's disease.

So consider that beta-amyloid is increased in the Alzheimer's not as a cause, but rather as an effect. This protein, the target of so many failed pharmaceutical campaigns, may well be our brain's desperate response to an invading organism, herpes simplex or who knows what else. So we should reconsider our thought process on what underlies this devastating disease, especially as it relates to the role of beta-amyloid. Remember, the enemy of my enemy is my friend.

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