Scientists have discovered that the body’s own immune alarms may play a major role in rapid-aging diseases.
Although cigarette smoking remains the main driver of COPD, e-cigarettes are also raising concerns. Vaping aerosols can contain nicotine, ultrafine particles and flavouring chemicals that may irritate the lungs and contribute to inflammation. The long-term effects are still unclear because these products are relatively new.
That matters particularly for younger people. In Great Britain, recent survey data suggest that 7% of 11-to 17-year-olds currently vape. While that does not mean they will go on to develop COPD, it does mean more young lungs are being exposed to substances whose long-term effects are not yet fully understood.
COPD is often diagnosed only after major lung damage has already occurred. Because it develops so gradually, people may dismiss early breathlessness, coughing or mucus production as a consequence of getting older, being unfit or smoking. Respiratory organisations warn that symptoms such as cough, phlegm and shortness of breath should not be treated as a normal part of ageing, while studies show that COPD remains widely underdiagnosed, including among people with respiratory symptoms.
In Aging Cell, researchers have elucidated the relationship between intestinal aging and age-related changes to the gut microbiome.
Two interdependent biologies
The human gut works through the interaction of two entirely different sets of cells. The first is the body’s actual cells, including the intestinal barrier between the gut and the rest of the body, various types of ordinary immune cells, and Peyer’s patches with follicle-associated epithelium (FAE) areas that contain microfold cells (M cells), which perform crucial immunoregulatory tasks [1]. The second is the gut microbiome, the various types of bacteria that help us digest food.
Researchers at the University of Rochester showed that one of those biological advantages can be moved into another mammal. By transferring a gene linked to the naked mole rat’s unusually high levels of high molecular weight hyaluronic acid (HMW-HA), the team improved health and modestly extended lifespan in mice.
The work, published in Nature in 2023, suggested that at least some longevity traits that evolved in long-lived animals may be adaptable beyond the species that developed them. The genetically modified mice lived healthier lives and had an approximate 4.4 percent increase in median lifespan compared with ordinary mice.
“Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals,” says Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester.
Diet and exercise are both factors that can influence how long you live, but they’re not the single greatest predictor of your longevity, research suggests.
According to a recent study, there’s something else that might have more of an effect in terms of curtailing your lifespan.
While poor sleep has been previously linked to a host of health issues, this latest investigation found that getting enough shut-eye had a stronger connection to living longer than diet and exercise – factors that are known to add years to your life.
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Cerebral amyloid angiopathy is a major cause of hemorrhagic stroke, a frequent contributor to age-related cognitive impairment, and a key component in adverse responses to beta-amyloid (Aβ) immunotherapy. Defined by pathological deposition of Aβ in the small blood vessels of the brain, cerebral amyloid angiopathy is most often diagnosed on the basis of magnetic resonance imaging studies showing multiple hemorrhages or leptomeningeal blood products within or overlying the cerebral cortex. The disorder typically manifests as hemorrhagic stroke or as a contributing factor to cognitive decline and, less commonly, with transient focal neurologic symptoms or a cerebral inflammatory autoimmune syndrome.
In a recently published review, researchers led by Prof. Wu Qingfeng at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences explored the ongoing process of neural cell competition (NCC), a fundamental mechanism that shapes the brain across the lifespan.
The review is published in National Science Review, and provides fresh insights into how brain cells continuously “compete” for survival and how this competition impacts brain development, wiring, function, and aging.
Although neural cell competition is widely recognized for its role during early brain development, Prof. Wu’s team demonstrated that this process continues to be vital throughout life. They revealed that NCC not only helps maintain healthy brain function but also contributes to age-related cognitive decline when disrupted.