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Cellular Senescence In Ageing And Neurodegenerative Disorders: Molecular Mechanisms, Biomarkers, And Therapeutic Strategies

Aging Theory
Aging Pathway
Therapeutic
Cellular senescence, a process where cells stop dividing and accumulate in tissues, is increasingly recognized as a key contributor to aging and the development of neurodegenerative disorders like Alzheimer’s and Parkinson’s diseases.
Author

Gemini

Published

November 4, 2026

As we age, our bodies undergo many changes, and sometimes, individual cells can enter a state called “cellular senescence.” These senescent cells stop dividing and, instead of dying off, they linger and can release harmful substances, creating a toxic environment for surrounding healthy cells. This process is now understood to play a significant role in how our brains age and in the progression of debilitating conditions such as Alzheimer’s, Parkinson’s, and ALS.

Researchers are actively investigating the specific ways these “zombie cells” contribute to brain damage, including how their secretions, known as the “senescence-associated secretory phenotype” (SASP), trigger chronic inflammation and harm neurons. Identifying these senescent cells is crucial, and scientists are working on developing reliable markers to detect them.

The good news is that new therapeutic strategies are emerging. These include “senolytics,” which are drugs designed to selectively eliminate senescent cells, and “senomorphics,” which aim to neutralize the harmful substances these cells release. While there are still challenges in bringing these treatments from the lab to patients, particularly in targeting specific cell types and finding effective biomarkers, the potential to combat age-related neurodegenerative diseases by tackling cellular senescence is a promising area of research.


Source: link to paper