Alzheimer's Drugs Worsen Memory Loss
April 21, 2010 S. L. Baker
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."