Geroscience: Linking Aging to Chronic Disease

In the citing paper

“Chronological age is the major predictor for most of the diseases that account for the bulk of morbidity, mortality and health costs across low-, middle- and high-income countries2–7.”

In the citing paper

“The Geroscience Hypothesis holds that these pillars of aging, including cellular senescence, tend to progress in concert and may be root-cause contributors to the pathophysiology of multiple diseases”

In the citing paper

“Old age is the greatest risk factor for the chronic diseases responsible for the majority of morbidity, mortality, and health-care costs worldwide (1, 2).”

In the citing paper

“Recent studies of animal models have established the veracity of the geroscience hypothesis (1).”

In the citing paper

“Interlinked and fundamental aging processes appear to be a root-cause contributor to many disorders and diseases.”

In the citing paper

“The recognition that old age is the greatest risk factor for most chronic diseases led to the geroscience hypothesis, which posits that therapeutically targeting fundamental aging mechanisms will successfully impact multiple chronic diseases because these diseases all share the same underlying mechanism (1).”

In the citing paper

“This hypothesis posits that by targeting a fundamental ageing process such as cellular senescence, multiple age-related disorders can be delayed, prevented, or alleviated as a group, instead of one-at-a-time.”

In the citing paper

“The geroscience hypothesis proposes that therapy to slow or reverse molecular changes that occur with aging can delay or prevent multiple chronic diseases and extend healthy lifespan1–3.”

In the citing paper

“Evidence amassed in recent years indicates that aging science shows great promise as a method of extending health span (50)(51)(52)(53)(54)(55)(56).”

In the citing paper

“The somewhat surprising finding is that DNA damage has far-reaching effects on many aspects of cellular metabolism tied to aging, the so-called pillars of aging (Kennedy et al., 2014).”

In the citing paper

“Senescent cells expressing this phenotype can in turn promote a multitude of chronic health conditions and diseases, including insulin resistance, CVD, pulmonary arterial hypertension, chronic obstructive pulmonary disorder, emphysema, Alzheimer’s and Parkinson’s diseases, macular degeneration, osteoarthritis and cancer54,55.”

In the citing paper

“Paramount among them is the accumulation of senescent cells in multiple tissues.”

In the citing paper

“Thus, PA and exercise may be considered central geriatric care interventions, that is, interventions that act on the cellular and molecular drivers of biological aging to decelerate the rates of aging, which constitute the basics of the geroscience field [633,634].”

In the citing paper

“Thus, PA and exercise may be considered central geriatric care interventions, that is, interventions that act on the cellular and molecular drivers of biological aging to decelerate the rates of aging, which constitute the basics of the geroscience field [633,634].”

In the citing paper

“The hallmarks of aging are interconnected (Kennedy et al., 2014; López-Otín et al., 2013; Zhang et al., 2015a), and age-associated perturbations of one can affect others.”

In the citing paper

“Over the past decades, a large body of research has shown that the molecular and cellular decline of aging can be organized into several evolutionarily conserved hallmarks or pillars of aging (Kennedy et al., 2014; López-Otín et al., 2013).”

In the citing paper

“time‐dependent loss of autophagy proficiency is thought to critically contribute to the aged phenotype (Lopez‐Otin et al, 2013; Kennedy et al, 2014; Lopez‐Otin & Kroemer, 2021)”

In the citing paper

“The molecular causes of physical aging are thought to occur through the accumulation of cellular damage to mitochondrial DNA (mtDNA), telomeric ends, coding-DNA, and proteins (Kennedy et al, 2014).”

In the citing paper

“Ageing is also characterized by the appearance of different chronic diseases such as sarcopenia, type 2 diabetes mellitus (T2DM), cardiovascular disease, hypercholesterolemia, hypertension or neurodegenerative diseases among others (Kennedy et al., 2014).”

In the citing paper

“Ageing is multifactorial involving different molecular and cellular processes such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intracellular communication (Kennedy et al., 2014; Lopez-Otin et al., 2013).”

In the citing paper

“The geroscience hypothesis posits that interventions that target key hallmarks of aging potentially can prevent, delay, or even reverse age-related conditions as a group (1).”

In the citing paper

“Biological ageing is enormously complex and is thought to be driven by the interaction of multiple dysregulated cellular and biochemical processes3,4.”

In the citing paper

“Indeed, it could be argued that, as much of the basic biology of ageing seems largely conserved among many species with very different lifespans3,4,8, clocks that measure a universal cause or rate of ageing should function ubiquitously.”