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Ageism, a form of social discrimination targeted specifically at older adults, is pervasive in our society, but its negative impact on the well-being of older persons is rarely recognized and its causes and consequences are not sufficiently understood. In this issue, we present a collection of review and opinion articles on the theme of ageism that all speak to the need and ways to create an anti-ageist future. Our cover image demonstrates the fallacy that older adults form a monolithic group with regards to interests and capabilities, and reinforces a sense of optimism for achieving a positive attitude toward old age.
The consequences of ageism have never been more apparent than in the context of a global pandemic. In this special issue on ageism, Nature Aging demonstrates its commitment to supporting efforts to combat ageism in all its forms.
Ahead of the release of the global report on ageism, the World Health Organization calls for everyone to take action to change the way we think, feel and act towards age and aging.
When older workers are discriminated against, everyone is affected. Age discrimination negatively impacts not only individual workers but also their families and the broader economy, argues Joo Yeoun Suh.
To be anti-ageist is to be self-educating, calling out discrimination wherever we see it and being uncompromising in our demand for full dignity and citizenship for everyone at every stage of life, argues Dr Alexandre Kalache, president of the International Longevity Centre-Brazil.
COVID-19 has highlighted pervasive ageism and the interconnectedness of individuals and societies. This Comment discusses how creating an anti-ageist healthcare system will improve health outcomes for our current and future selves.
Mitochondrial dysfunction can result in numerous diseases, including neurodegenerative disorders. CBP/p300, a histone acetyltransferase, has been uncovered as a key factor in the response to mitochondrial perturbation. It controls transcription of mitochondrial stress response genes, promotes innate immunity and enhances longevity.
Accelerated aging and cellular senescence are driving forces of pulmonary fibrosis. A novel anti-aging therapeutic approach combats lung fibrosis by targeting senescent fibrogenic cells for apoptosis.
In this issue of Nature Aging, Janbek et al. report results of a registry-based cohort study in Denmark where older people with incident dementia had higher risk of infections, especially in the nervous system. They call for interventions for better health and quality of life for people living with dementia.
Despite scarce evidence, ageism is often cited as a social factor contributing to elder mistreatment. This Perspective examines the limited research linking these issues and proposes a model and research agenda to further understand the relationship.
Stressed mitochondria activate multiple defense pathways to improve health. Li et al. show that the acetyltransferases CBP/p300 play a central role in mitochondrial stress signaling that defends mitochondrial function and promotes health and longevity.
Investigation of the long-lived blind mole rat adaptive immune system reveals that they do not accumulate large memory T-cell clones and effector programs with aging. Such organization could relieve the burden of inflammaging triggered by persistent clonal expansions and contribute to the long and healthy Spalax lifespan.
The authors identify an atypical type of stem cell division that regulates hair follicle organ homeostasis and aging in mice. These ‘stress-responsive-type’ asymmetrical cell divisions cause hair follicle stem cells to detach from the basement membrane leading to their exhaustion, elimination and organ aging.
Using a mouse model of lung fibrosis, the authors find that overexpression of SIRT3 in myofibroblasts lowers their threshold for apoptosis, allowing their clearance from tissues and restoration of the lost capacity for fibrosis resolution in aged mice.
The authors show that plasma levels of NfL increase with age in humans and are associated with mortality in nonagenarians and centenarians. In mice, a life-extending dietary restriction manipulation attenuated the similar age-related increase in plasma NfL levels.
In a nationwide, longitudinal and population-based matched-cohort study, Janbek and colleagues find dementia to be a risk factor for infection-related hospital contacts and conclude that infections might be an early sign of dementia.