Senescent cells accumulate with age in tissues throughout the body, generating sustained pro-inflammatory signaling that is increasingly disruptive to tissue structure and function. This is an important contribution to degenerative aging, as illustrated by the many animal studies in which senolytic therapies that selectively destroy senescent cells produce significant reversal of aspects of aging and age-related disease. Here, researchers review the evidence for senolytic therapies to effectively treat neurodegenerative conditions by removing the harms done by senescent cells in the brain.
The cellular phenomenon of aging is irreversible and is characterized by the arrest of cell division and induction of growth. It is believed that this mechanism contributes to age-related illnesses, such as neurodegenerative diseases, as well as the ageing process itself. The ability of aging cells in the brain to release pro-inflammatory chemicals like cytokines and chemokines is a factor that contributes to the deterioration of neurons and the advancement of neurodegenerative disorders. The accumulation of β-amyloid and tau proteins seen in Alzheimer’s disease (AD), coupled with the clustering of senescent microglia and astrocytes in the brain, worsens neuroinflammation. Similarly, the accumulation of senescent dopaminergic neurons and microglia has been accompanied by the pathogenesis of Lewy bodies and the neuroinflammatory response in individuals with Parkinson’s disease (PD).
Current research has looked at the possibility of alleviating the symptoms of neurodegenerative diseases by using senolytics, which are pharmaceuticals or chemical compounds that selectively remove aged cells. In animal models of AD and PD, senolytic therapy has been demonstrated to enhance cognitive function and decrease neuroinflammation in both diseases. Despite the promising potential of targeting cellular senescence, several challenges remain. Further research is needed to better understand the complex interplay between senescent cells and the surrounding microenvironment in the brain. Additionally, the long-term safety and efficacy of senolytic therapies need to be carefully evaluated in clinical trials.
