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"Animals Longevity."
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Methuselah's zoo : what nature can teach us about living longer, healthier lives
\"A natural history of longevity in a wide variety of species along with an exploration of what we can learn from other species to preserve and extend human health\"-- Provided by publisher.
Book
Social isolation shortens lifespan through oxidative stress in ants
Social isolation negatively affects health, induces detrimental behaviors, and shortens lifespan in social species. Little is known about the mechanisms underpinning these effects because model species are typically short-lived and non-social. Using colonies of the carpenter ant
Camponotus fellah
, we show that social isolation induces hyperactivity, alters space-use, and reduces lifespan via changes in the expression of genes with key roles in oxidation-reduction and an associated accumulation of reactive oxygen species. These physiological effects are localized to the fat body and oenocytes, which perform liver-like functions in insects. We use pharmacological manipulations to demonstrate that the oxidation-reduction pathway causally underpins the detrimental effects of social isolation on behavior and lifespan. These findings have important implications for our understanding of how social isolation affects behavior and lifespan in general.
The mechanisms behind the negative effects of social isolation on social species are unclear. Here, the authors examine colonies of carpenter ants, finding that behavioral, physiological, and lifespan changes may be caused by oxidative stress.
Journal Article
Extreme longevity : discovering Earth's oldest organisms
\"Some creatures can outlive humans by centuries. Readers will learn about these extreme examples of longevity in the animal kingdom, how aging happens, and what genes help animals to live so long\"-- Provided by publisher.
Book
Increased hyaluronan by naked mole-rat Has2 improves healthspan in mice
Abundant high-molecular-mass hyaluronic acid (HMM-HA) contributes to cancer resistance and possibly to the longevity of the longest-lived rodent—the naked mole-rat
1
,
2
. To study whether the benefits of HMM-HA could be transferred to other animal species, we generated a transgenic mouse overexpressing naked mole-rat hyaluronic acid synthase 2 gene (nmr
Has2
). nmr
Has2
mice showed an increase in hyaluronan levels in several tissues, and a lower incidence of spontaneous and induced cancer, extended lifespan and improved healthspan. The transcriptome signature of nmr
Has2
mice shifted towards that of longer-lived species. The most notable change observed in nmr
Has2
mice was attenuated inflammation across multiple tissues. HMM-HA reduced inflammation through several pathways, including a direct immunoregulatory effect on immune cells, protection from oxidative stress and improved gut barrier function during ageing. These beneficial effects were conferred by HMM-HA and were not specific to the nmr
Has2
gene. These findings demonstrate that the longevity mechanism that evolved in the naked mole-rat can be exported to other species, and open new paths for using HMM-HA to improve lifespan and healthspan.
Mice overexpressing
Has2
from the naked mole-rat showed an increase in hyaluronan levels in several tissues, and a lower incidence of spontaneous and induced cancer, attenuated inflammation through several pathways, extended lifespan and improved healthspan.
Journal Article
Extending the human lifespan
\"At Issue: Extending the Human Lifespan: Books in this anthology series focus a wide range of viewpoints onto a single controversial issue, providing in-depth discussions by leading advocates, a quick grounding in the issues, and a challenge to critical thinking skills\"-- Provided by publisher.
Book
Circadian autophagy drives iTRF-mediated longevity
Time-restricted feeding (TRF) has recently gained interest as a potential anti-ageing treatment for organisms from
Drosophila
to humans
1
–
5
. TRF restricts food intake to specific hours of the day. Because TRF controls the timing of feeding, rather than nutrient or caloric content, TRF has been hypothesized to depend on circadian-regulated functions; the underlying molecular mechanisms of its effects remain unclear. Here, to exploit the genetic tools and well-characterized ageing markers of
Drosophila
, we developed an intermittent TRF (iTRF) dietary regimen that robustly extended fly lifespan and delayed the onset of ageing markers in the muscles and gut. We found that iTRF enhanced circadian-regulated transcription and that iTRF-mediated lifespan extension required both circadian regulation and autophagy, a conserved longevity pathway. Night-specific induction of autophagy was both necessary and sufficient to extend lifespan on an ad libitum diet and also prevented further iTRF-mediated lifespan extension. By contrast, day-specific induction of autophagy did not extend lifespan. Thus, these results identify circadian-regulated autophagy as a critical contributor to iTRF-mediated health benefits in
Drosophila
. Because both circadian regulation and autophagy are highly conserved processes in human ageing, this work highlights the possibility that behavioural or pharmaceutical interventions that stimulate circadian-regulated autophagy might provide people with similar health benefits, such as delayed ageing and lifespan extension.
Circadian-regulated autophagy contributes to the health benefits of intermittent time-restricted feeding in
Drosophila
.
Journal Article
Promoting Drp1-mediated mitochondrial fission in midlife prolongs healthy lifespan of Drosophila melanogaster
The accumulation of dysfunctional mitochondria has been implicated in aging, but a deeper understanding of mitochondrial dynamics and mitophagy during aging is missing. Here, we show that upregulating Drp1—a Dynamin-related protein that promotes mitochondrial fission—in midlife, prolongs
Drosophila
lifespan and healthspan. We find that short-term induction of Drp1, in midlife, is sufficient to improve organismal health and prolong lifespan, and observe a midlife shift toward a more elongated mitochondrial morphology, which is linked to the accumulation of dysfunctional mitochondria in aged flight muscle. Promoting Drp1-mediated mitochondrial fission, in midlife, facilitates mitophagy and improves both mitochondrial respiratory function and proteostasis in aged flies. Finally, we show that autophagy is required for the anti-aging effects of midlife Drp1-mediated mitochondrial fission. Our findings indicate that interventions that promote mitochondrial fission could delay the onset of pathology and mortality in mammals when applied in midlife.
Mitochondrial fission and fusion are important mechanisms to maintain mitochondrial function. Here, the authors report that middle-aged flies have more elongated, or ‘hyper-fused’ mitochondria, and show that induction of mitochondrial fission in midlife, but not in early life, extends the health and life of flies.
Journal Article
Mitonuclear protein imbalance as a conserved longevity mechanism
Longevity is regulated by a network of closely linked metabolic systems. We used a combination of mouse population genetics and RNA interference in
Caenorhabditis elegans
to identify mitochondrial ribosomal protein S5 (
Mrps5
) and other mitochondrial ribosomal proteins as metabolic and longevity regulators. MRP knockdown triggers mitonuclear protein imbalance, reducing mitochondrial respiration and activating the mitochondrial unfolded protein response. Specific antibiotics targeting mitochondrial translation and ethidium bromide (which impairs mitochondrial DNA transcription) pharmacologically mimic
mrp
knockdown and extend worm lifespan by inducing mitonuclear protein imbalance, a stoichiometric imbalance between nuclear and mitochondrially encoded proteins. This mechanism was also conserved in mammalian cells. In addition, resveratrol and rapamycin, longevity compounds acting on different molecular targets, similarly induced mitonuclear protein imbalance, the mitochondrial unfolded protein response and lifespan extension in
C. elegans
. Collectively these data demonstrate that
MRPs
represent an evolutionarily conserved protein family that ties the mitochondrial ribosome and mitonuclear protein imbalance to the mitochondrial unfolded protein response, an overarching longevity pathway across many species.
Mitochondrial ribosomal proteins have been identified as longevity regulators in
C. elegans
and mammalian systems, their role in longevity is linked to mitonuclear protein imbalance and the mitochondrial unfolded protein response.
MRP
gene family linked to longevity
Animals vary dramatically in lifespan, but why is not clear. Here Johan Auwerx and colleagues report how natural variation in mitochondrial ribosome protein expression translates to lifespan extension in mice and worms, and suggest a unified mechanism behind the effects of metabolic perturbations on longevity. They looked for genetic variation linked to longevity in the BXD genetic reference population of inbred mouse strains. Longevity mapped to mitochondrial ribosomal proteins. Using mouse population genetics and RNA interference experiments in
Caenorhabditis elegans
, mitochondrial ribosomal protein S5 (Mrps5) and other mitochondrial ribosomal proteins were identified as metabolic and longevity regulators.
Journal Article
An open science study of ageing in companion dogs
The Dog Aging Project is a long-term longitudinal study of ageing in tens of thousands of companion dogs. The domestic dog is among the most variable mammal species in terms of morphology, behaviour, risk of age-related disease and life expectancy. Given that dogs share the human environment and have a sophisticated healthcare system but are much shorter-lived than people, they offer a unique opportunity to identify the genetic, environmental and lifestyle factors associated with healthy lifespan. To take advantage of this opportunity, the Dog Aging Project will collect extensive survey data, environmental information, electronic veterinary medical records, genome-wide sequence information, clinicopathology and molecular phenotypes derived from blood cells, plasma and faecal samples. Here, we describe the specific goals and design of the Dog Aging Project and discuss the potential for this open-data, community science study to greatly enhance understanding of ageing in a genetically variable, socially relevant species living in a complex environment.
The Dog Aging Project is an open-data, community science study to identify genetic, environmental and lifestyle factors associated with canine healthy lifespan, generating knowledge that could readily translate to human ageing.
Journal Article
Autophagy in aging and longevity
Our understanding of the process of autophagy and its role in health and diseases has grown remarkably in the last two decades. Early work established autophagy as a general bulk recycling process which involves the sequestration and transport of intracellular material to the lysosome for degradation. Currently, autophagy is viewed as a nexus of metabolic and proteostatic signalling that can determine key physiological decisions from cell fate to organismal lifespan. Here, we review the latest literature on the role of autophagy and lysosomes in stress response and longevity. We highlight the connections between autophagy and metabolic processes, the network associated with its regulation, and the links between autophagic dysfunction, neurodegenerative diseases, and aging.
Journal Article