Aging is a preoccupation shared by beauty bloggers, serious journalists, scientists, doctors, celebrities—arguably all of adult America, given the pervasiveness of the crusade against it in popular ...culture and the media. We take our youth-oriented culture as a given but, as Lawrence R. Samuel argues, this was not always the case. Old age was revered in early America, in part because it was so rare. Indeed, it was not until the 1960s, according to Samuel, that the story of aging in America became the one we are most familiar with today: aging is a disease that science will one day cure, and in the meantime, signs of aging should be prevented, masked, and treated as a source of shame.By tracing the story of aging in the United States over the course of the last half century, Samuel vividly demonstrates the ways in which getting older tangibly contradicts the prevailing social values and attitudes of our youth-obsessed culture. As a result, tens of millions of adults approaching their sixties and seventies in this decade do not know how to age, as they were never prepared to do so.Despite recent trends that suggest a more positive outlook, getting old is still viewed in terms of physical and cognitive decline, resulting in discrimination in the workplace and marginalization in social life. Samuels concludes Aging in America by exhorting his fellow baby boomers to use their economic clout and sheer numbers to change the narrative of aging in America.
Featured Cover Zane, Flaminia; Bouzid, Hayet; Sosa Marmol, Sofia ...
Aging cell,
11/2023, Letnik:
22, Številka:
11
Journal Article
Recenzirano
Odprti dostop
Cover legend: The cover image is based on the Research Article Smurfness‐based two‐phase model of ageing helps deconvolve the ageing transcriptional signature by Flaminia Zane et al., ...https://doi.org/10.1111/acel.13946 Image Credit: Michael Rera and Aurore Colibert
The development of frailty scores suitable for mice and which resemble those used in the clinical scenario is of great importance to understand human frailty. The aim of the study was to determine an ...individual frailty score for each mouse at different ages and analyze the association between the frailty score and its lifespan. For this purpose, the "Valencia Score" for frailty was used. Thus, a longitudinal study in mice was performed analyzing weight loss, running time and speed, grip strength and motor coordination at the late-adult, mature and old ages (40, 56 and 80 weeks old, respectively). These parameters are equivalent to unintentional weight loss, poor endurance, slowness, weakness, and low activity level, respectively, in humans. A cut-off point was used to identify frail mice for each criterion. All the measurements were also performed on chronologically adult prematurely aging mice. The results show that by using the "Valencia Score" for frailty a prematurely aged phenotype can be identified even during the adulthood of animals. This opens up the possibility of carrying out preventive long-term interventions. Moreover, the individual frailty score of a given mouse at the late-adult, mature and old ages is shown to be a relevant predictor of its lifespan.
For several decades, understanding ageing and the processes that limit lifespan have challenged biologists. Thirty years ago, the biology of ageing gained unprecedented scientific credibility through ...the identification of gene variants that extend the lifespan of multicellular model organisms. Here we summarize the milestones that mark this scientific triumph, discuss different ageing pathways and processes, and suggest that ageing research is entering a new era that has unique medical, commercial and societal implications. We argue that this era marks an inflection point, not only in ageing research but also for all biological research that affects the human healthspan.
Ageing of the immune system, or immunosenescence, contributes to the morbidity and mortality of the elderly
. To define the contribution of immune system ageing to organism ageing, here we ...selectively deleted Ercc1, which encodes a crucial DNA repair protein
, in mouse haematopoietic cells to increase the burden of endogenous DNA damage and thereby senescence
in the immune system only. We show that Vav-iCre
;Ercc1
mice were healthy into adulthood, then displayed premature onset of immunosenescence characterized by attrition and senescence of specific immune cell populations and impaired immune function, similar to changes that occur during ageing in wild-type mice
. Notably, non-lymphoid organs also showed increased senescence and damage, which suggests that senescent, aged immune cells can promote systemic ageing. The transplantation of splenocytes from Vav-iCre
;Ercc1
or aged wild-type mice into young mice induced senescence in trans, whereas the transplantation of young immune cells attenuated senescence. The treatment of Vav-iCre
;Ercc1
mice with rapamycin reduced markers of senescence in immune cells and improved immune function
. These data demonstrate that an aged, senescent immune system has a causal role in driving systemic ageing and therefore represents a key therapeutic target to extend healthy ageing.
PDF
