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"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
Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances
We use a genome-wide association of 1 million parental lifespans of genotyped subjects and data on mortality risk factors to validate previously unreplicated findings near CDKN2B-AS1, ATXN2/BRAP, FURIN/FES, ZW10, PSORS1C3, and 13q21.31, and identify and replicate novel findings near ABO, ZC3HC1, and IGF2R. We also validate previous findings near 5q33.3/EBF1 and FOXO3, whilst finding contradictory evidence at other loci. Gene set and cell-specific analyses show that expression in foetal brain cells and adult dorsolateral prefrontal cortex is enriched for lifespan variation, as are gene pathways involving lipid proteins and homeostasis, vesicle-mediated transport, and synaptic function. Individual genetic variants that increase dementia, cardiovascular disease, and lung cancer – but not other cancers – explain the most variance. Resulting polygenic scores show a mean lifespan difference of around five years of life across the deciles. Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter ). Ageing happens to us all, and as the cabaret singer Maurice Chevalier pointed out, \"old age is not that bad when you consider the alternative\". Yet, the growing ageing population of most developed countries presents challenges to healthcare systems and government finances. For many older people, long periods of ill health are part of the end of life, and so a better understanding of ageing could offer the opportunity to prolong healthy living into old age. Ageing is complex and takes a long time to study – a lifetime in fact. This makes it difficult to discern its causes, among the countless possibilities based on an individual’s genes, behaviour or environment. While thousands of regions in an individual’s genetic makeup are known to influence their risk of different diseases, those that affect how long they will live have proved harder to disentangle. Timmers et al. sought to pinpoint such regions, and then use this information to predict, based on their DNA, whether someone had a better or worse chance of living longer than average. The DNA of over 500,000 people was read to reveal the specific ‘genetic fingerprints’ of each participant. Then, after asking each of the participants how long both of their parents had lived, Timmers et al. pinpointed 12 DNA regions that affect lifespan. Five of these regions were new and had not been linked to lifespan before. Across the twelve as a whole several were known to be involved in Alzheimer’s disease, smoking-related cancer or heart disease. Looking at the entire genome, Timmers et al. could then predict a lifespan score for each individual, and when they sorted participants into ten groups based on these scores they found that top group lived five years longer than the bottom, on average. Many factors beside genetics influence how long a person will live and our lifespan cannot be read from our DNA alone. Nevertheless, Timmers et al. had hoped to narrow down their search and discover specific genes that directly influence how quickly people age, beyond diseases. If such genes exist, their effects were too small to be detected in this study. The next step will be to expand the study to include more participants, which will hopefully pinpoint further genomic regions and help disentangle the biology of ageing and disease.
Journal Article
The price of immortality : the race to live forever
\"As longevity medicine revolutionizes the lives of many older people, the quest to take the next step--to live as long as we choose--has spurred a scientific arms race in search of the elixir of life, funded by Big Tech and Silicon Valley. It has also empowered a wild-eyed fringe of pseudo-scientists, tech visionaries, scam-artists, and religious fanatics who have given their lives over to the pursuit of immortality. Starting off at the Church of Perpetual Life in Florida and exploring the feuding subcultures around the cryonics industry, Peter Ward immerses himself into an eccentric world of startups, scam artists, scientific institutions, and tech billionaires to deliver this deeply reported, nuanced, and sometimes very funny exploration of the race for immortality--and the potentially devastating consequences should humanity realize its ultimate dream\"-- 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
The oldest living things in the world
\"The Oldest Living Things in the World is an epic journey through time and space. Over the past decade, artist Rachel Sussman has researched, worked with biologists, and traveled the world to photograph continuously living organisms that are 2,000 years old and older. Spanning from Antarctica to Greenland, the Mojave Desert to the Australian Outback, the result is a stunning and unique visual collection of ancient organisms unlike anything that has been created in the arts or sciences before, insightfully and accessibly narrated by Sussman along the way...Alongside the photographs, Sussman relays fascinating -- and sometimes harrowing -- tales of her global adventures tracking down her subjects and shares insights from the scientists who research them. The oldest living things in the world are a record and celebration of the past, a call to action in the present, and a barometer of our future.\" -- Publisher's description.
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
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
Interventions to Slow Aging in Humans: Are We Ready?
Summary The workshop entitled 'Interventions to Slow Aging in Humans: Are We Ready?' was held in Erice, Italy, on October 8-13, 2013, to bring together leading experts in the biology and genetics of aging and obtain a consensus related to the discovery and development of safe interventions to slow aging and increase healthy lifespan in humans. There was consensus that there is sufficient evidence that aging interventions will delay and prevent disease onset for many chronic conditions of adult and old age. Essential pathways have been identified, and behavioral, dietary, and pharmacologic approaches have emerged. Although many gene targets and drugs were discussed and there was not complete consensus about all interventions, the participants selected a subset of the most promising strategies that could be tested in humans for their effects on healthspan. These were: (i) dietary interventions mimicking chronic dietary restriction (periodic fasting mimicking diets, protein restriction, etc.); (ii) drugs that inhibit the growth hormone/IGF-I axis; (iii) drugs that inhibit the mTOR-S6K pathway; or (iv) drugs that activate AMPK or specific sirtuins. These choices were based in part on consistent evidence for the pro-longevity effects and ability of these interventions to prevent or delay multiple age-related diseases and improve healthspan in simple model organisms and rodents and their potential to be safe and effective in extending human healthspan. The authors of this manuscript were speakers and discussants invited to the workshop. The following summary highlights the major points addressed and the conclusions of the meeting.
Journal Article