My paternal grandmother gradually lost her memory up to the point she was basically as functional as a newborn baby. According to the National Institute on Aging, about 5% of men and women between the age of 65 and 74 have Alzheimer’s disease, and about half of those 85 and older may have the disease.
In his book Ending Aging, biogerontologist Aubrey de Grey explains that Alzheimer’s is a disease related to aging, caused by damage that accumulates with time and, at a certain age, reaches a threshold that turns it into a pathology. The cause is most likely the accretion of beta-amyloids in the brain, a type of mis-folded protein.
The implications are that we’ll all get Alzheimer’s if something else doesn’t kill us first, and as our life expectancy rises, the risk goes up.
So this disease is one of the challenges standing in the way of curing aging (and reducing human suffering in general), and defeating it is something that we could all benefit from. This is why I encourage you to donate to the Methuselah Foundation and join a distributed computing project that works on computational protein design like Rosetta@Home (join my team here), or protein folding (and mis-folding) like Folding@Home.
But don’t despair! There’s some good news:
Arun Ghosh, at right, and Xiaoming Xu. Credit: Purdue University.
A molecule designed by a Purdue University researcher to stop the debilitating symptoms of Alzheimer’s disease has been shown in its first phase of clinical trials to be safe and to reduce biomarkers for the disease.
CoMentis, the pharmaceutical company developing the drug, announced on Jan. 7 completion of its Phase 1 study of a treatment based on the molecule. Results from the study indicate that the treatment is safe and well tolerated. […]
The molecule, called a beta-secretase inhibitor, prevents the first step in a chain of events that leads to amyloid plaque formation in the brain. This plaque formation creates fibrous clumps of toxic proteins that are believed to cause the devastating symptoms of Alzheimer’s.
The study of 48 healthy volunteers showed dose-related reduction in plasma amyloid beta, a protein believed to be a key biomarker of Alzheimer’s. Results showed a single dose of the drug produced a greater than 60 percent reduction of the biomarker. Subjects received one of six different doses or a placebo, and the study measured levels of the therapeutic drug and levels of the biomarker in the bloodstream.
CoMentis plans to begin a phase II clinical study of the drug, oral CTS-21166, in Alzheimer’s patients in 2008.
It’s too early to tell if this specific drug will work, but the goal certainly is to clean up the damage in the brain before it leads to Alzheimer’s. A cure for people who already have the disease would be fantastic, but the real goal is to avoid getting it in the first place.
- Purdue-designed Alzheimer’s treatment completes first phase of testing
- Research could lead to treatment for Alzheimer’s disease
- Amyloid Beta at Wikipedia
- Alzheimer’s disease at Wikipedia