Cellular senescence is referred to as the permanent arrest of cells. It occurs when the cells are no longer able to undergo cell division.

Among several factors that promote the onset of senescence are DNA damage, neuroinflammation, oxidative stress, and altered proteostasis.

Senescent cells contribute to the impairment of tissue regeneration, cellular dysfunction, and impact on the microenvironment. A study has noted that the heightened presence of senescent cells leads to the pathophysiology of neurodegenerative diseases.

Oxidative stress and neuroinflammation contribute to accelerated aging and cognitive dysfunction stages. It is implicated in the progression of cognitive decline, neuronal degeneration, and synapse loss during later life stages.

On the other hand, eliminating senescent cells affects wound healing and possibly the development of the placenta and the embryo, tumor suppression, and plays a pathological role in age-related diseases.

Previous studies in mice have shown that the elimination of senescent cells improves brain function in neurodegenerative diseases. However, whether senescent cell clearance during the aging process alleviates cognitive dysfunction is still unknown.

Read the original publication of this study here: [ Whole-body senescent cell clearance alleviates age-related brain inflammation and cognitive impairment in mice ]

Learn how eliminating senescent cells in aging improved cognitive function and reduced brain impairment, as suggested by this study in aged mice.

Small-experimental-mouse-is-on-the-laboratory-----…--as-suggested-by-this-study-in-aged-mice | Elimination of Senescent Cells Improves Cognitive Function in Neurodegenerative Diseases Caused by Aging

Whole-body senescent cell clearance alleviates age-related brain inflammation and cognitive impairment in mice.

Researchers from Mayo Clinic conducted single-nuclei and single-cell RNA-seq in the hippocampus from young and aged mice to investigate the effects of senescent cell clearance in cognitive dysfunction during the aging process.

Findings of this study indicate that senescent cell removal in aged mice improves cognitive ability in animals with signs of dementia.

During the initial observation, an age-dependent increase in p16Ink4a senescent cells, a protein involved in the regulation of the cell cycle, was more pronounced in microglia and oligodendrocyte progenitor cells. These were characterized by a senescence-associated secretory phenotype (SASP), which functions to link cell senescence to various biological processes.

To genetically eliminate the p16Ink4a -positive senescent cells, the aged mice were treated with the drug AP20187 and either with AP20187 or with the senolytic cocktail Dasatinib and Quercetin.

Based on this method, the researchers observed that both strategies resulted in a decrease in p16Ink4a exclusively in the microglial population, resulting in reduced microglial activation and reduced expression of SASP factors.

These approaches to eliminate senescent cells have been shown to improve cognitive function in aged mice significantly. Senolytic drugs may potentially prove to be effective, mechanism‐based interventions for alleviating chronic brain disease such as Alzheimer’s disease.

This study provides proof-of-concept for therapies that selectively destroy senescent cells in old tissues can be a potential therapeutic intervention to alleviate cognitive impairment related to aging.


  1. Whole-body senescent cell clearance alleviates age-related brain inflammation and cognitive impairment in mice ]
  2. Physiological and pathological consequences of cellular senescence ]
  3. Cellular Senescence in Neurodegenerative Diseases ]
  4. Cellular senescence in aging and age-related diseases: Implications for neurodegenerative diseases ]