Topic collection

Aging

What changes with age and whether those changes can be measured or slowed.

13 articles

A translucent freshwater hydra with an elongated body, long tentacles, and a developing lateral bud against a dark background.

Aging6 min read

The surprising evidence for aging in Hydra oligactis

Hydras are famous for regeneration and their apparent resistance to aging. But a long-term study of Hydra oligactis found rising mortality with age, better survival under reduced feeding, and a negative association between tumour development and survival.

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A large and a small dog beside a DNA visualization showing different levels of epigenetic regulation over mobile genomic elements.

Aging5 min read

Why big dogs live shorter lives: an epigenetic clue

An analysis of 1,640 methylomes from 894 dogs found that larger dogs age faster at the molecular level. Size-related changes were especially pronounced at transposable elements, including LINE1 sequences.

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An older adult exercising on a stationary bicycle, with extracellular vesicles carrying microRNA-29 illustrated traveling toward cartilage in the knee joint.

Aging5 min read

How exercise protects cartilage: a microRNA-29 signal

A Nature Aging study traces one molecular route from aerobic exercise to aging cartilage. Exercise altered extracellular-vesicle cargo, with microRNA-29 helping restore healthier chondrocyte features through the KL/α-Klotho pathway.

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Cells from the same mouse tissue displaying visibly different gene-activity states, represented as a transition from younger-looking to older-looking cellular profiles.

Aging5 min read

Age of individual mouse cells can be estimated from gene activity

scMLEAge estimates age-related states of individual cells from gene-expression profiles. Cells from the same mouse can receive different transcriptomic ages, revealing substantial heterogeneity within a tissue.

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A mouse beside a DNA double helix showing fewer newly arising mutations under calorie restriction.

Aging4 min read

Calorie restriction and mutations: what mice revealed

Mice consuming about 30% fewer calories accumulated fewer somatic mutations across several tissues. Unexpectedly, the largest reduction appeared in relatively inactive regions of the genome.

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Histology sections from several human organs arranged along a timeline with different periods of accelerated structural change.

Aging4 min read

Human organ aging follows different structural schedules

An analysis of 25,306 samples from 40 tissues found that structural aging is not uniform across the body. Vascular tissues changed fastest in the 30s, while other organs accelerated later or in two distinct phases.

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Aging5 min read

DREAM complex and aging: a brake on DNA repair

The DREAM complex suppresses DNA-repair genes. Its activity has now been linked to somatic mutation burden, mammalian lifespan and the severity of age-related neuropathology.

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DNA mutations may limit longevity even without other ageing mechanisms.

Aging5 min read

Somatic mutations and ageing: where longevity may hit a limit

A mathematical model asks how long humans might live if every other ageing mechanism were removed. Somatic mutation mainly limited lifespan through poorly renewable cells in the brain and heart.

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Why we age even though much of the body is constantly renewing itself seems like a genuine biological paradox. Cells at the surface of the skin are replaced, the intestinal lining continually regenerates, and bone is remodeled throughout life. If worn-out parts can be replaced, why doesn't the body periodically reset its age? Because cellular renewal is not the same thing as restoring the organism to its original state. ## Renewal is not a biological reset A new cell does not appear from nowhere. In renewing tissues, it is typically produced by another cell, often a stem or progenitor cell. DNA must be copied, cellular structures distributed, the appropriate genes activated, and the new cell integrated into an existing tissue. All of this takes place inside an organism that is itself changing with time. As we age, cells accumulate DNA damage and somatic mutations, while chromatin organization and patterns of gene activity change. Systems that maintain proteins in the correct state become less efficient, and damaged molecules and cellular components are not always removed as effectively. Mitochondria, which participate in energy metabolism and many signaling pathways, also undergo age-related changes. A newly produced cell therefore does not mean a newly produced organism. It is created within a biological system that already carries the history of previous decades. Nor are all cells continually replaced. Some cell populations are exceptionally long-lived, including many neurons. These cells may have to maintain themselves for decades, repairing damage rather than simply being exchanged for new copies. ## The cells, their environment, and the repair system all age Aging also changes the machinery responsible for tissue renewal. Stem cells allow many organs to replenish their cellular populations, but stem cells and the environments that support them also change over time. One of the processes included in modern frameworks of aging is stem cell exhaustion: the regenerative capacity of some tissues gradually declines. At the same time, senescent cells become increasingly important. These are cells that have entered a state in which they no longer divide normally but do not necessarily die. Cellular senescence can be useful. It can prevent a damaged cell from continuing to proliferate and can contribute to processes such as wound healing. The problem arises when senescent cells persist. They can release numerous signaling molecules that alter the behavior of surrounding cells. When they accumulate, they may contribute to chronic inflammation and disturb normal tissue function. The environment around cells also changes. Immune activity, hormonal signals, metabolism, inflammatory pathways, and the gut microbiota all form part of the biological setting in which cells operate. A newly generated cell is therefore placed not into a young body, but into a tissue with a particular biological history. ## Aging has no single cause In 2013, Carlos López-Otín and colleagues proposed an influential framework describing nine “hallmarks of aging”: interconnected biological processes that characterize and help explain aging. A decade later, the authors revised the framework. Their 2023 review in Cell proposed twelve hallmarks. Some involve the maintenance of biological information, including genomic instability, telomere attrition, and epigenetic alterations. Others concern cellular quality control, such as loss of proteostasis and impaired macroautophagy, the process through which cells remove and recycle damaged components. Aging is also associated with changes in nutrient sensing and mitochondrial function. Cellular senescence and stem cell exhaustion affect how tissues maintain and regenerate themselves. At the organismal level, altered communication between cells, chronic inflammation, and changes in the microbiome are also included in the updated framework. These twelve hallmarks should not be interpreted as twelve independent failures. They interact extensively. DNA damage can promote cellular senescence; senescent cells can help sustain inflammation; chronic inflammation can then alter the environment in which many other cells function. This is why modern biology does not reduce aging to a single defective pathway, an “aging gene,” or one type of molecular damage. The twelve-hallmark framework is not a final map of aging either. It is a conceptual model that integrates a large body of experimental evidence, much of it obtained from cells and model organisms. It is useful for organizing mechanisms and generating hypotheses, but it does not mean that targeting any single hallmark will necessarily rejuvenate a person or extend human lifespan. The apparent paradox therefore disappears. The body does repair and renew itself throughout life, but it does not dismantle itself and rebuild from an untouched blueprint. New cells are produced within a system that is aging at the same time. The body is constantly being repaired. But repair never returns the entire system exactly to its starting point.

Aging5 min read

Why we age even though the body keeps renewing itself

Skin, intestinal tissue, and bone are continually renewed, yet the body still ages. We explain why replacing cells does not reset biological age and how cells, tissues, and repair systems change over time.

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A three-dimensional brain map with colored regions indicating areas that appear younger or older than expected on MRI

Aging5 min read

What local brain age reveals about uneven aging

A deep-learning model replaced a single brain-age estimate with a detailed regional map, revealing distinct patterns in healthy aging, mild cognitive impairment and Alzheimer’s disease.

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Гиппокамп человеческого мозга, клетки микроглии и сложенная внутри клеточного ядра молекула ДНК.

Aging5 min read

How the human hippocampus ages: An immune shift after 50

A single-cell analysis of hippocampal tissue from 40 adults aged 20 to 95 revealed a major midlife shift in microglial identity, a declining proportion of astrocytes, and weakening three-dimensional genome organization.

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Стареющие иммунные клетки в центре силуэта человека направляют воспалительные сигналы к печени, почкам и лёгким.

Aging4 min read

How an Aging Immune System May Accelerate Aging Across the Body

With age, the immune system not only responds less effectively to infection but also sustains chronic inflammation. A major review examines how aged immune cells may spread dysfunction to other organs.

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Filtered coffee, instant coffee, and a DNA-filled hourglass representing differences in biological aging associated with coffee preparation methods.

Aging4 min read

Instant and Filtered Coffee Show Opposite Links to Biological Aging

Two cups of coffee may look similar while containing quite different mixtures of chemicals. A large UK Biobank analysis suggests that those differences may also matter for biological aging.…

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