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Previous studies have shown that the aging process is characterized by a gradual decline in memory, attention control, orientation and cognition.
In addition, aging is a major risk factor for the development of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), primary aggressive multiple sclerosis (PPMS), Alzheimer's disease (AD) and Parkinson's disease (PD).
cell aging is characterized by irreversible cell cycle stagnation and inflammatory aging-related secretion esotypes (SASP), which is a major factor in aging and age-related diseases.
in mouse models of neurodegenerative diseases, removing senescing cells has been shown to improve brain function.
, it remains to be seen whether the removal of senescing cells will alleviate cognitive impairments in the aging process.
to study the problem, the researchers first conducted single-nucleo and single-celled RNA-seq in the sea mass of young and old mice.
it observed an increase in age dependence on p16Ink4a senescing cells, which is more pronounced in small glial cells and less progeny glial cell progeny cells, which are characterized by the secretion of SASP.
then, the researchers treated ink-ATTAC mice with aging and treated them with AP20187 or a cocktail therapy that removes senescies, Dasatinib and Quercetin.
researchers observed that both strategies led to a decrease in p16Ink4a specificity in the small glial group, resulting in a decrease in the activation of the small glial and a decrease in SASP factor expression.
, both methods significantly improved cognitive function in older mice.
, this data provides proof of concept for removing senescellular interventions as a potential treatment for age-related cognitive impairment.