When the new Alzheimer’s drug bapineuzumab was first introduced, the headlines read,
“Bapineuzumab Results Encouraging.” However, the most recent study found that the drug provided no benefit to 1,300 subjects who lacked a gene that is associated with Alzheimer’s.
Bapineuzumab functions by breaking up a protein in the brain called beta amyloid, which is found in patients suffering from Alzheimer’s disease. Many research studies have correlated beta amyloid with the development of Alzheimer’s. However, an association does not always mean causation.
When I read that the drug was designed to clear beta amyloid from the brain, I was not optimistic that it would work. By the time beta amyloid is forming, it’s too late.
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Instead of developing a drug to treat the beta amyloid, we should put our research money behind studies that can identify what we need to do to prevent beta amyloid protein from forming in the first place.
So how does beta amyloid develop in the brain? That’s the million-dollar question that needs to be answered in order to create an effective treatment plan for Alzheimer’s disease.
One theory is that beta amyloid forms as a response to injury and inflammation. It is the brain’s way of trying to heal. But if brains cells do not have the ability to properly protect and heal from injury, damage from beta amyloid protein can develop.
How can you ensure that the brain has the correct balance of nutrients to maintain optimal
function and has the ability to heal from injury? The answer is easy: eat a good diet, maintain optimal nutrient and hormonal levels, keep hydrated, and detoxify from heavy metals.
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