Disease drivers of aging

Hodes, Richard J.; Sierra, Felipe; Austad, Steven N.; Epel, Elissa S.; Neigh, Gretchen N.; Erlandson, Kristine M.; Schafer, Marissa J.; LeBrasseur, Nathan K.; Wiley, Christopher D.; Campisi, Judith; Sehl, Mary E.; Scalia, Rosario; Eguchi, Satoru; Kasinath, Balakuntalam S.; Halter, Jeffrey B.; Cohen, Harvey Jay; Demark‐Wahnefried, Wendy; Ahles, Tim A.; Barzilai, Nir; Hurria, Arti; Hunt, Peter W.

doi:10.1111/nyas.13299

Cited by 108 publications

(89 citation statements)

References 161 publications

(262 reference statements)

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“…2 in Ref. ). A central feature of this model is a decline of β cell function and insulin secretion with aging, consistently observed in rodents and humans .…”

Section: Diseases Accelerate the Appearance Of Aging Phenotypes In Humentioning

confidence: 97%

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Kohanski

Deeks

Gravekamp

et al. 2016

Annals of the New York Academy of Sciences

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Aging is the major risk factor for both the development of chronic diseases and loss of functional capacity. Geroscience provides links among the biology of aging, the biology of disease, and the physiology of frailty, three fields where enormous progress has been made in the last few decades. While, previously, the focus was on the role of aging in susceptibility to disease and disability, the other side of this relationship, which is the contribution of disease to aging, has been less explored at the molecular/cellular level. Indeed, the role of childhood or early adulthood exposure to chronic disease and/or treatment on accelerating aging phenotypes is well known in epidemiology, but the biological basis is poorly understood. A recent summit co-organized by the National Institutes of Health GeroScience Interest Group and the New York Academy of Sciences explored these relationships, using three chronic diseases as examples: cancer, HIV/AIDS, and diabetes. The epidemiological literature clearly indicates that early exposure to any of these diseases and/or their treatments results in an acceleration of the appearance of aging phenotypes, including loss of functional capacity and accelerated appearance of clinical symptoms of aging-related diseases not obviously related to the earlier event. The discussions at the summit focused on the molecular and cellular relationships between each of these diseases and the recently defined molecular and cellular pillars of aging. Two major conclusions from the meeting include the desire to refine an operational definition of aging and to concomitantly develop biomarkers of aging, in order to move from chronological to physiological age. The discussion also opened a dialogue on the possibility of improving late-life outcomes in patients affected by chronic disease by including age-delaying modalities along with the standard care for the disease in question.

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“…2 in Ref. ). A central feature of this model is a decline of β cell function and insulin secretion with aging, consistently observed in rodents and humans .…”

Section: Diseases Accelerate the Appearance Of Aging Phenotypes In Humentioning

confidence: 97%

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Kohanski

Deeks

Gravekamp

et al. 2016

Annals of the New York Academy of Sciences

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“…Epidemiological studies have found that inflammageing is a risk factor for CVD, cancer, chronic kidney disease, dementia, and depression as well for global indicators of poor health status, such as multimorbidity, mobility disability and disability in activities of daily living, sarcopenia, frailty, and premature death 9–19 . On the basis of these findings, many researchers have proposed that inflammageing is a marker of accelerated ageing and should be considered to be one of the pillars of the biology of ageing 20 . The root causes of inflammageing are poorly understood, as are the mechanisms that connect inflammageing with CVD and with many other health outcomes.…”

Section: Risk Factors and Causes Of Inflammageingmentioning

confidence: 99%

Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty

2018

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Most older individuals develop inflammageing, a condition characterized by elevated levels of blood inflammatory markers that carries high susceptibility to chronic morbidity, disability, frailty, and premature death. Potential mechanisms of inflammageing include genetic susceptibility, central obesity, increased gut permeability, changes to microbiota composition, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by dysfunctional mitochondria, immune cell dysregulation, and chronic infections. Inflammageing is a risk factor for cardiovascular diseases (CVDs), and clinical trials suggest that this association is causal. Inflammageing is also a risk factor for chronic kidney disease, diabetes mellitus, cancer, depression, dementia, and sarcopenia, but whether modulating inflammation beneficially affects the clinical course of non-CVD health problems is controversial. This uncertainty is an important issue to address because older patients with CVD are often affected by multimorbidity and frailty — which affect clinical manifestations, prognosis, and response to treatment — and are associated with inflammation by mechanisms similar to those in CVD. The hypothesis that inflammation affects CVD, multimorbidity, and frailty by inhibiting growth factors, increasing catabolism, and interfering with homeostatic signalling is supported by mechanistic studies but requires confirmation in humans. Whether early modulation of inflammageing prevents or delays the onset of cardiovascular frailty should be tested in clinical trials.

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“…This effort was done in conjunction with the New York Academy of Sciences, and it was focused on the opposite side of the coin: what are the molecular and cellular mechanisms that explain why certain diseases can lead to an acceleration of the aging process? A report from the effort is currently in press (Hodes et al 2016). …”

Section: Early Activitiesmentioning

confidence: 99%

Geroscience and the trans-NIH Geroscience Interest Group, GSIG

2017

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Age is by far the major risk factor for most chronic diseases. This has been common knowledge since time immemorial. Aging encompasses the biological changes most often seen as declines of function and increasing burden of disease. The close linkage of these two has led people to believe that aging, like age, is immutable. It is only recently that research into the basic molecular and cellular mechanisms of aging has led to potential interventions that increase lifespan and appear to increase healthspan, as well. Geroscience is an interdisciplinary field that aims to understand the relationship between the biology of aging and the biology of age-related diseases. The Bgeroscience hypothesisp osits that manipulation of aging will delay (in parallel) the appearance or severity of many chronic diseases because these diseases share the same underlying major risk factor (age). The hope is that this will lead to health improvements in the older population with perhaps greater efficiency than can be achieved through the successful cure and management of diseases of aging as they arise individually or as comorbidities.With those concepts in mind, the Geroscience Interest Group (GSIG) was launched as a trans-institute interest group within the NIH in November 2012. Here, we discuss the genesis of the trans-NIH group and the most salient activities that have occurred in the last 5 years.

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Disease drivers of aging

Cited by 108 publications

References 161 publications

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty

Geroscience and the trans-NIH Geroscience Interest Group, GSIG

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