Scientists may have found a new way to slow Alzheimer’s disease by helping brain cells repair their own DNA.
The discovery, published in FEBS Open Bio, comes from researchers at King’s College London, who tested an experimental drug called KCL-286 in mice with Alzheimer’s disease. The results suggest that fixing damage inside brain cells could become a new treatment strategy.
Alzheimer’s disease is the most common cause of dementia. It slowly destroys brain cells, leading to memory loss, confusion, difficulty thinking, and problems carrying out everyday tasks.
Current treatments mainly help manage symptoms or slow disease progression, but they do not stop the disease. Scientists are therefore searching for new approaches that target the underlying causes.
One possible cause is DNA damage. DNA contains the genetic instructions that allow every cell to function properly.
Brain cells, called neurons, are expected to last for a lifetime, but over many years they can accumulate damage caused by aging, inflammation, harmful molecules, and normal body processes. When this damage builds up faster than it can be repaired, neurons may stop working properly or eventually die.
The research team focused on a protein called retinoic acid receptor-beta, or RARβ. This protein helps control which genes are switched on or off. The experimental drug KCL-286 activates this receptor. Once activated, it starts a chain of events that encourages the cell to produce more DNA repair proteins, helping damaged neurons fix their genetic material.
The scientists tested KCL-286 in a mouse model of Alzheimer’s disease. After treatment, the mice showed better repair of DNA damage inside neurons. The drug also reduced inflammation in the brain and lowered abnormal activity of immune cells that are believed to contribute to Alzheimer’s disease. Together, these changes may help protect brain cells from further injury.
Professor Jonathan Corcoran compared the process to repairing potholes in a road. Once the damage is repaired, normal traffic can flow again. In the same way, repairing DNA damage may allow brain cells to function more normally and reduce harmful inflammation.
The researchers believe this approach could eventually help treat not only Alzheimer’s disease but also other conditions involving nerve damage or neurodegeneration. Because DNA damage occurs in many neurological disorders, improving the brain’s natural repair systems could have wide-ranging benefits.
Importantly, this research was performed in mice, not people. Many treatments that work well in animals do not always succeed in human clinical trials. However, there is encouraging news.
Early phase 1 clinical trials have already shown that KCL-286 appears to have a good safety profile in humans. If funding becomes available, larger clinical studies can begin to test whether the drug improves memory, thinking, and daily functioning in people with Alzheimer’s disease.
Overall, this study introduces an exciting new direction in Alzheimer’s research. Rather than focusing only on amyloid or tau proteins, it aims to repair damage that may contribute to disease progression. The study’s strengths include identifying a clear biological target and demonstrating benefits in an animal model.
Its main limitation is that it has not yet shown effectiveness in patients. Larger human trials will be needed before doctors know whether this promising treatment can become part of future Alzheimer’s care.
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Source: King’s College London.
