Drug restores senescent cell clearance in aging mice

A study in mice suggests that blocking a specific receptor can restore the body's ability to clear senescent cells, leading to healthier aging outcomes including better memory and reduced frailty.

Researchers led by Katrin Andreasson at Stanford University compared young and old mice and identified that elevated prostaglandin E2 overstimulates the EP2 receptor on macrophages, impairing clearance of senescent neutrophils.

Genetically modifying the EP2 gene in older mice improved their ability to remove these cells. The animals showed lower inflammation, less muscle loss, reduced visceral fat, better mobility and near-normal performance on memory tests.

An experimental oral drug that blocks EP2 produced similar benefits after two months of treatment in older mice. Human liver samples displayed comparable patterns of higher EP2 activity and more senescent neutrophils.

Derek Gilroy of University College London called the findings promising but noted that broader EP2 blockade could cause unwanted effects. The team plans further studies on links to conditions such as Alzheimer’s disease.

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Vivid illustration of human neurons showing enhanced DNA repair linked to the APOE2 variant, for a news article on aging research.
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Study links APOE2 variant to stronger DNA repair and reduced cellular aging in human neurons

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A study from the Buck Institute for Research on Aging reports that the APOE2 variant—long associated with lower Alzheimer’s risk and exceptional longevity—helps human neurons better withstand DNA damage and resist a senescent, dysfunctional state. The work, published in the journal Aging Cell, used engineered human stem-cell–derived neurons and mouse models to explore how common APOE gene forms may influence cellular stress responses.

Researchers at Cold Spring Harbor Laboratory have found that blocking the protein PTP1B improves memory and boosts plaque clearance in mouse models of Alzheimer's disease. The discovery links the protein to brain immune function and metabolic risks like diabetes and obesity. The team aims to develop inhibitors for potential human treatments.

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Researchers have identified declining levels of phosphatidylcholine as a key driver of age-related mitochondrial dysfunction. The discovery, made at the Leibniz Institute on Aging in Germany, shows that boosting this lipid can restore youthful mitochondrial function in laboratory models.

Researchers from the Institute for Bioengineering of Catalonia and collaborating institutions report that engineered “supramolecular” nanoparticles restored aspects of blood-brain barrier function in Alzheimer’s-model mice, rapidly lowering brain amyloid-β and producing improvements on behavioral and memory tests.

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A widely studied anti-aging treatment triggered significant brain damage in mice, according to new research from the University of Connecticut. The drug combination dasatinib plus quercetin caused myelin loss and changes resembling those seen in multiple sclerosis. The findings raise questions about its use in longevity studies and off-label therapies.

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