Rapamycin improves healthspan but not inflammaging in nf κb1−/− mice

In this study, we investigated whether rapamycin could ameliorate age‐associated phenotypes in a mouse model of genetically enhance d NF‐κB activity (nf κb1−/−) characterized by low ‐grade chronic inflammation, accelerated aging and CLD. We found that, despite showing no beneficial effects in lifespan and inflammaging, rapamycin reduced frailty and improved long‐term memory, neuromuscular coordination and tissue architecture. Importantly, markers of cellular senescence, a k nown driver of age‐related pathology, were alleviated in rapamycin‐fed animals. Our results indicate that, in conditions of genetically enhanced NF‐κB, rapamycin delays aging phenotypes and improves healthspan uncoupled from its role as a suppressor of inflammation.

Source: Aging Cell - November 23, 2018 Category: Cytology Authors: Clara Correia ‐Melo, Jodie Birch, Edward Fielder, Dina Rahmatika, Jennifer Taylor, James Chapman, Anthony Lagnado, Bernadette M. Carroll, Satomi Miwa, Gavin Richardson, Diana Jurk, Fiona Oakley, Jelena Mann, Derek A. Mann, Viktor I. Korolc Tags: ORIGINAL PAPER Source Type: research