Researchers at the Indiana University School of Medicine have identified a promising new target for treating Alzheimer’s disease, raising hopes for future therapies that could slow or even prevent the condition’s progression.
Their work focuses on an enzyme in brain cells that appears to play a key role in the buildup of amyloid plaques, one of the main features of Alzheimer’s disease.
Alzheimer’s is a progressive brain disorder that affects memory, thinking, and behavior.
In recent years, two drugs—lecanemab and donanemab—have been approved to remove amyloid plaques from the brain.
These treatments can slow decline for some patients, but they do not stop the disease entirely. Scientists continue to search for new approaches that target the disease earlier and more effectively.
The Indiana University team, led by Dr. Hande Karahan and Dr. Jungsu Kim, studied an enzyme called IDOL.
They discovered that removing this enzyme from neurons, the brain cells responsible for communication, significantly reduced the amount of amyloid plaques in animal models of Alzheimer’s disease. This suggests that blocking IDOL could be a new way to protect the brain.
What surprised the researchers most was where the effect occurred. They initially expected the brain’s immune cells, known as microglia, to play the biggest role in clearing plaques.
Instead, removing the enzyme specifically from neurons had the strongest impact. This finding highlights the importance of neuron health in Alzheimer’s and suggests that treatments aimed directly at these cells may be especially beneficial.
The study also found that reducing IDOL lowered levels of a protein called apolipoprotein E, or APOE. One form of this protein, known as APOE4, is the strongest genetic risk factor for late-onset Alzheimer’s disease.
APOE is involved in how the brain processes fats and cholesterol, which are essential for healthy cell function. Changes in this protein may help explain how the new approach reduces plaque buildup and supports brain health.
In addition, removing the enzyme increased the number of certain receptors that help regulate both amyloid plaques and lipid metabolism in the brain.
These receptors are important for communication between neurons and may help the brain resist damage even after plaques have formed. Researchers believe this dual effect—reducing harmful plaques while strengthening the brain’s resilience—could lead to more effective treatments.
Another encouraging aspect of the discovery is that enzymes like IDOL are considered good drug targets. Their structure makes it possible to design medicines that attach precisely to them and block their activity, potentially reducing side effects.
The research team plans to continue studying ways to safely inhibit the enzyme and test whether doing so can preserve connections between brain cells and prevent other Alzheimer’s changes, such as the buildup of tau protein. Although the findings are still in early stages and based on animal studies, they open the door to a new direction in Alzheimer’s research.
Scientists hope that targeting this enzyme could one day lead to treatments that not only slow the disease but also protect brain function, offering new hope to patients and families affected by Alzheimer’s.
