Cellular Senescence In Neurodegenerative Diseases: A Bibliometric Analysis And Mechanistic Synthesis Linking Translational Pathways To Therapeutic Implications
As we age, our bodies undergo many changes, and sometimes, individual cells can enter a state called “cellular senescence.” These cells stop dividing, but they don’t die; instead, they become dysfunctional and can release a cocktail of inflammatory molecules, growth factors, and enzymes, collectively known as the “senescence-associated secretory phenotype” or SASP. This SASP can harm surrounding healthy cells and contribute to chronic inflammation.
Recent research highlights that these senescent cells accumulate in the brain as we get older and are now considered a significant factor in the development and progression of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Their presence can lead to the buildup of abnormal proteins, like those seen in Alzheimer’s, and fuel the chronic inflammation that damages brain tissue.
The good news is that understanding this process opens up exciting new possibilities for treatment. Scientists are exploring therapies that either selectively eliminate these senescent cells, called “senolytics,” or modify the harmful substances they release, known as “senomorphics.” Early studies suggest that clearing these problematic cells can improve brain function in models of neurodegenerative diseases. Targeting specific senescent brain immune cells, called microglia, is also emerging as a promising strategy to slow down the progression of these debilitating conditions.
Source: link to paper