Senolytics offer hope for more precise Alzheimer’s treatments

A new research paper has been published in Aging ((Aging-vs) On March 29, 2025, as the coverage of part 17, number 3, entitled “Differential Senolytic inhibition of normal versus AP-Associed cholinesterases: implications in aging and Alzheimer’s disease.”

In this study, a research team of Dalhousie University, led by Sultan Darvesh, that certain anti-aging connections, known as senolytics, can block harmful brain enzymes that are linked to Alzheimer’s disease (AD) without having a healthy influence. Senolytics are connections that help damaged or to clean up “zombie” cells that accumulate with age and contribute to inflammation and tissue disorders. This work provides new insight into how ad-related damage can be accurately directed, which means that the road is led for safer treatments that protect memory and brain health in older adults.

Alzheimer’s disease is one of the most common causes of memory loss and dementia. A characteristic of the disease is the structure of sticky protein clonts in the brain, known as amyloid-beta plaques. Two Enzymen-Acetylcholinesterase (Ache) and Butyrylcholinesterase (Bche)-were found near these plaques. Although these enzymes play an important role in brain function, they can also contribute to ad -progression when they attach themselves to plaques. Medicines that focus on these enzymes are already used to help with memory, but they often block both harmful and healthy forms, which can cause unwanted side effects.

To investigate a better solution, researchers tested six connections that are known for their anti-aging or brain reinforcement properties. They wanted to know whether these connections only form the harmful pain and bche and enzymes related to Alzheimer’s disease. With the help of brain tissue samples of AD patients and enzyme activity tests, they discovered that connections such as dasatinib and nintedanib, both senolytics, Were able to block the forms of Ache and Bche associated with amyloid-beta plaques. However, these connections had no influence on normal brain enzymes.

“We show that the selected senolytics and nootropic brakes Ches associated with plaques but not the enzymes associated with normal neural elements.”

The study also used computer modeling to investigate how these connections interact with the enzymes. The models showed that the enzymes change shape near plaques, making it easier for certain connections to focus. This change can explain how the medicines can only selectively influence the sick areas of the brain.

Although not all connections worked equally well, the findings offer a new strategy for the treatment of AD. By concentrating on the differences between healthy and sick enzyme forms, researchers can possibly design more accurately and effective therapies. This selective approach can improve memory, reduce inflammation and avoid the side effects of the current treatments of AD.

In summary, this study opens new possibilities for the treatment of Alzheimer’s disease in a more focused way. It also emphasizes how discoveries in aging and brain health can work together to create better therapies for neurodegenerative diseases.