Alzheimer’s disease is the most common cause of dementia and affects millions of people worldwide. It slowly damages memory, thinking, and the ability to carry out everyday tasks.
Although some newer medicines can slow the disease a little, there is still no cure, so scientists continue searching for better treatments.
A new study from King’s College London has identified a promising experimental drug called KCL-286 that may attack Alzheimer’s disease in a different way. The findings were based on studies in mice and suggest the drug may slow several of the earliest changes linked to the disease instead of focusing on just one problem.
The research was published by scientists from King’s College London. The team reported that KCL-286 had already completed Phase 1 clinical trials showing it was safe and well tolerated in people when it was being developed for spinal cord injury. This could shorten the time needed before larger studies in Alzheimer’s patients begin.
For many years, Alzheimer’s research has mainly focused on two proteins called amyloid-beta and tau. These proteins build up inside the brain and are believed to contribute to the loss of brain cells. However, treatments that only target amyloid have produced only modest benefits for many patients.
The researchers wanted to investigate other changes that happen much earlier in the disease. Previous studies have shown that inflammation and damage to DNA appear before severe memory loss develops. These early changes may help drive the disease and could be important treatment targets.
In mouse models of Alzheimer’s disease, KCL-286 repaired damaged DNA and reduced inflammation in the brain. By improving both problems at the same time, the drug showed the potential to slow the disease process rather than simply treating symptoms after they appear.
The drug works by activating a protein involved in the retinoic acid pathway, which helps the body use vitamin A. Earlier studies suggested problems in this pathway may contribute to the development of amyloid deposits in the brain. The new research found that activating the pathway also helped repair dangerous breaks in DNA.
The scientists explained that DNA double-strand breaks are among the most serious forms of DNA damage because both strands are broken. If these breaks are not repaired, brain cells may stop working properly or die. KCL-286 appeared to improve the cells’ ability to repair this damage.
The research team became interested in Alzheimer’s after earlier work found similarities between spinal cord injury and Alzheimer’s disease. Since KCL-286 had already shown benefits in repairing nerve cell damage after spinal cord injury, the scientists believed it might also help protect brain cells affected by Alzheimer’s.
The findings are encouraging, but they should be interpreted carefully because they come from animal studies rather than human patients. Many treatments that work well in mice do not always succeed in people.
Even so, the fact that KCL-286 has already passed an early human safety study makes it an especially interesting candidate for future clinical trials. If larger studies confirm these results, the drug could become a new type of treatment that targets several causes of Alzheimer’s disease at once instead of focusing on only one.
If you care about Alzheimer’s disease, please read studies about the protective power of dietary antioxidants against Alzheimer’s, and eating habits linked to higher Alzheimer’s risk.
For more health information, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.
Source: King’s College London.
