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Open AccessJournal ArticleDOI

Canonical Nlrp3 Inflammasome Links Systemic Low-Grade Inflammation to Functional Decline in Aging

TLDR
Nlrp3 inflammasome is revealed as an upstream target that controls age-related inflammation and an innovative therapeutic strategy to lower NLRp3 activity to delay multiple age- related chronic diseases is offered.
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Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases

TL;DR: The session on inflammation of the Advances in Gerosciences meeting held at the National Institutes of Health/National Institute on Aging in Bethesda on October 30 and 31, 2013 was aimed at defining these important unanswered questions about inflammaging.
Journal ArticleDOI

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

TL;DR: Whether therapies to modulate inflammageing can reduce the age-related decline in health is discussed, and the hypothesis that inflammation affects CVD, multimorbidity, and frailty is supported by mechanistic studies but requires confirmation in humans.
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Ageing as a risk factor for neurodegenerative disease.

TL;DR: Hallmarks of ageing — genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication — correlate with susceptibility to neurodegenerative disease.
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The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease

TL;DR: In vivo, BHB or a ketogenic diet attenuates caspase-1 activation and IL-1β secretion in mouse models of NLRP3-mediated diseases such as Muckle–Wells syndrome, familial cold autoinflammatory syndrome and urate crystal–induced peritonitis and the findings suggest that the anti-inflammatory effects of caloric restriction or ketogenic diets may be linked to BHB-mediated inhibition of theNLRP3 inflammasome.
References
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Journal ArticleDOI

Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease

TL;DR: These findings suggest a sequence of events in the pathogenesis of AD in which Aβ induces membrane-associated oxidative stress, resulting in perturbed ceramide and cholesterol metabolism which, in turn, triggers a neurodegenerative cascade that leads to clinical disease.
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Mitochondria and the autophagy-inflammation-cell death axis in organismal aging

TL;DR: In this paper, a combination of mitochondrial dysfunction and insufficient autophagy may contribute to multiple aging-associated pathologies, which can cause degenerative diseases in which deficient quality control results in inflammation and the death of cell populations.
Journal ArticleDOI

Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes

TL;DR: T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response, and increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM.
Journal ArticleDOI

Innate immunity in the central nervous system

TL;DR: The cellular and molecular basis of innate immunity in the CNS is reviewed and what is known about how outcomes of these interactions can lead to resolution of infection, neurodegeneration, or neural repair depending on the context is discussed.
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