Alzheimer's drugs cause brain damage and actually worsen memory loss
by S. L. Baker, features writer
(NaturalNews) Big Pharma drugs that are being used on humans right now and promoted as potential treatments for Alzheimer's disease (AD) could cause the very brain damage and memory loss they are supposed to treat. That's the conclusion of University of California at San Diego (UCSD) scientists who just published their groundbreaking findings in the Proceedings of the National Academy of Sciences.
The researchers combined several high tech methods to investigate nonamyloidogenic peptides that are formed by some drugs being tested as Alzheimer's therapies. UCSD nano-biophysicist Ratnesh Lal and his colleagues combined three dimensional computer simulations with high resolution atomic force microscopy membrane protein and cell imaging, electrical recording and various cellular assays to pinpoint the function of these substances.
The results showed that the peptides created active ion channels that caused brain cells to take in very high levels of calcium ions, eventually killing the very neurons needed for memory. To make matters worse, biomedical researchers have long considered these brain cell-killing nonamyloidogenic peptides to be non-toxic and targeted them as potential Alzheimer's treatments.
The UCSD researchers call their discovery that these peptides may be pathogenic (disease-causing) "startling" and say it may require new evaluations into the causes of AD and Down's Syndrome (which often causes Alzheimer's disease symptoms by age 40).
Clearly, the new findings are a blow to the widely accepted hypothesis that amyloid beta peptides must cause AD because amyloid plaques (consisting of deteriorating neurons surrounding deposits of a sticky protein called beta-amyloid) are found in the brains of AD patients.
Big Pharma researchers have developed drugs that are supposed to treat AD by increasing non-toxic peptides, thereby decreasing the impact of the "bad" peptides which generate beta-amyloid. Instead, they've only ended up producing more brain-damaging peptides.
"There are several drugs to treat Alzheimer's in Trials I and II, but we don't believe that they will be adopted for clinical usage," Dr. Lal, a joint professor in the UCSD Jacobs School of Engineering's Department of Mechanical and Aerospace Engineering and Bioengineering, said in a statement to the media. "We believe we are providing the most direct mechanism of Alzheimer's disease and Down Syndrome pathology. Through our research we have provided a structure and mechanism (an ion channel) that can account for the pathology. The strategy to control the activity of this structure -- the opening and closing of the channel --should be targeted for an effective treatment."