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The molecular inflammation hypothesis of aging proposes that redox dysregulation causes an age-related activation of NF-κB and its signaling to upregulate various proinflammatory genes.
The findings are consistent with the default – executive coupling hypothesis of aging and identify this shift in network dynamics as a candidate neural mechanism associated with crystalized cognition in later life that may signal adaptive capacity in the context of declining fluid cognitive abilities.
10 reference datasets were generated to test for the hypothesis of age-dependent changes in the ratios of non-synonymous to synonymous or RNA to synonymous.
Cross-resistance to multiple stresses and the lifespan-extending effects associated with mild exposures to these stresses is the basis for the "hormesis hypothesis" of aging [33].
Based on the free-radical hypothesis of ageing, we predict that sexually mature males should have an enhanced production of mitochondrial ROS associated with a less efficient antioxidant barrier, increasing their chronic level of oxidative damages.
Of note, most of them are closely associated with oxidative damage and metabolism, supporting the pathogenesis hypothesis of age-related dysfunction.
More importantly, we identified the pathway that related to the oxidative damage and ROS metabolism, supporting the pathogenesis hypothesis of age-related dysfunction.
Remarkably, most of them are associated with the oxidative stress, metabolism and degenerative nerve diseases, supporting the pathogenesis hypothesis of age-related dysfunction (Table 1).
Brunk and Terman [ 66] called this cellular status as "garbage can" hypothesis of aging.
This concept is based on the free radical hypothesis of aging as proposed by Harman [ 1].
Oxidative stress theory is now a more accepted hypothesis of aging [ 26].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com