Are Plaques Protective for Alzheimer's?
There’s a new kid on the block concerning Alzheimer’s theory. It is a surprising turn of the screw. Until now Alzheimer’s drugs have been targeting plaques. Could plaques actually be protective and might Alzheimer’s drugs be attacking the wrong enemy? Apparently, many researchers are now claiming that plaques trap and neutralize protein toxins, based on mice and rat studies. Instead of sticky plaques, free-floating bits of a toxic protein called amyloid beta may be what's killing off brain cells in Alzheimer's patients.
"If you say Alzheimer's, everyone immediately thinks that it's the plaques that actually cause the disease. That couldn't be further from the truth," Andrew Dillin, of the Salk Institute in California and the Howard Hughes Medical Institute explained at a conference on aging in May 2010."The data actually suggest these plaques are a form of protection that the body tries to put on. So this is a sign that your brain was trying to do something very useful and helpful to you, and the remnant was the formation of amyloid plaques." (Reuters)
Many of the old drugs don’t seem to be helpful and might accordingly be doing some harm! A new drug in late stage clinical trials at Pfizer, bapineuzumab is so far showing little effect based on this new scientific route. Bapineuzumab has had mixed results in a mid-stage clinical trial and some researchers were encouraged because it does reduce plaque levels in patients. But if you look at Dillin’s analysis then this new drug, like others which try to stop plaques from forming, is in his words, “destined to fail.” He continues, "This hypothesis is actually completely wrong, and we need a new way to start looking at this disease. This is actually not a viable therapeutic avenue."
This breakthrough might be just what the doctor ordered – a powerful reevaluation and new direction for research. If researchers are doing the same old, there will not be any different results. Meanwhile patients need to speak to their doctors because the drugs they might be taking could be causing more damage according to this research. In other words: The drugs attack the plaques, but the plaques protect brain cells from the protein clumps. I am excited about this kind of failure because it just might be the next step to the cure.
"If you say Alzheimer's, everyone immediately thinks that it's the plaques that actually cause the disease. That couldn't be further from the truth," Andrew Dillin, of the Salk Institute in California and the Howard Hughes Medical Institute explained at a conference on aging in May 2010."The data actually suggest these plaques are a form of protection that the body tries to put on. So this is a sign that your brain was trying to do something very useful and helpful to you, and the remnant was the formation of amyloid plaques." (Reuters)
Many of the old drugs don’t seem to be helpful and might accordingly be doing some harm! A new drug in late stage clinical trials at Pfizer, bapineuzumab is so far showing little effect based on this new scientific route. Bapineuzumab has had mixed results in a mid-stage clinical trial and some researchers were encouraged because it does reduce plaque levels in patients. But if you look at Dillin’s analysis then this new drug, like others which try to stop plaques from forming, is in his words, “destined to fail.” He continues, "This hypothesis is actually completely wrong, and we need a new way to start looking at this disease. This is actually not a viable therapeutic avenue."
This breakthrough might be just what the doctor ordered – a powerful reevaluation and new direction for research. If researchers are doing the same old, there will not be any different results. Meanwhile patients need to speak to their doctors because the drugs they might be taking could be causing more damage according to this research. In other words: The drugs attack the plaques, but the plaques protect brain cells from the protein clumps. I am excited about this kind of failure because it just might be the next step to the cure.
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