As researchers move closer to understanding how Alzheimer's disease (AD) develops, the prospect of medications designed to prevent or delay the devastating mental decline of AD has become more feasible. This week, research appearing in the current issue of the journal Science expands upon past work and may point the way toward effective treatments. With their research, German scientists demonstrate a new method for preventing the accumulation of beta-amyloid plaque— protein fragments believed to harm nerve cells— that may play a key role in the symptoms of AD.
The study, conducted by researchers from the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, concentrated on the activity of beta-secretase, an enzyme that slices proteins and results in the formation of neural plaques associated with AD. By inhibiting beta-secretase, researchers believe they may be able to prevent plaques from developing, and this theory has been the focus of many studies. In the past, researchers have designed drugs that work outside of affected cells, although the enzyme's action occurs within cells, and the German team sought to create a drug that would target the enzyme more directly. They combined a beta-secretase inhibitor with a molecule designed to secure it to the cell membrane, which would then allow it to affect the activity of enzymes within cells, and assessed its effectiveness using lab mice and fruit flies. In tests, a drug composed of the inhibitor alone was ineffective, but the combination of the inhibitor and the anchoring molecule resulted in a 50 percent decrease in neural plaques during a four-hour period.
While these results are promising, they are also preliminary, and further work is necessary to discover if this new method will be effective in humans. As more studies have investigated potential treatments for AD, researchers have met with disappointments, and the information gained from unsuccessful attempts at reversing mental decline should not be overlooked. In another recent study of a vaccine meant to fight the effects of AD, researchers found that while the vaccine did indeed reduce levels of neural plaque, it did not significantly improve cognitive ability. Although research has shown that plaques and tangles are characteristic of AD, no study has established a causal link, and the true nature of these abnormal protein deposits has yet to be determined. Further research may find that reducing plaque before the onset of symptoms is of some benefit, or that a treatment to decrease plaque levels will be most beneficial in combination with other treatments. Factors that we have not yet addressed may play a significant role in AD, and researchers need to continue searching for the mechanisms involved in this disease.
The German team plans to further study their new treatment model and predict that, if subsequent tests are successful, a version could be available for humans within ten years. In the current study, lab animals received the drug via an injection directly into the brain, and studies must now show that the drug can cross the blood-brain barrier, which would mean it could be given in the form of a pill or standard injection. Their work may be an important step forward in preventing or slowing the progress of AD, and as research continues to expand our understanding of AD, effective treatments will become a more likely possibility.
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