Increasing Cellular Energy Slows Aging Through Redox Signaling

See bolded below.

More cellular energy production, less aging and neuroinflammation!

Sarcopenia results essentially from decreased energy production, not from lack of combustible food or oxygen but due to mitochondrial dysfunction and lack of maintenance. 

BDNF is a bio marker of longevity and restorative gene expression.  

Increased HRV index is a functional marker of longevity and restorative gene effects.

Highlights

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  Mitochondrial hypometabolism, perturbed redox homeostasis, and chronic neuroinflammation characterize brain aging and Alzheimer’s disease
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  Increasing evidence from basic and clinical studies suggests that redox control serves as a bidirectional link between energy metabolism and inflammatory responses in the brain
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  This review focuses on the brain metabolic-inflammatory axis entailing the alterations in energy metabolism and inflammatory responses and their interconnected cross-talks via redox regulation in brain aging and Alzheimer’s disease

http://www.sciencedirect.com/science/article/pii/S0891584916302167

Energy Metabolism and Inflammation in Brain Aging and Alzheimer’s Disease

This review focuses on the brain metabolic-inflammatory axis entailing the alterations in energy metabolism and inflammatory responses and their interconnected cross-talks via redox regulation in brain aging and Alzheimer’s disease

The high energy demand of the brain renders it sensitive to changes in energy fuel supply and mitochondrial function. Deficits in glucose availability and mitochondrial function are well-known hallmarks of brain aging and are particularly accentuated in neurodegenerative disorders such as Alzheimer’s disease. As important cellular sources of H₂O₂, mitochondrial dysfunction is usually associated with altered redox status. Bioenergetic deficits and chronic oxidative stress are both major contributors to cognitive decline associated with brain aging and Alzheimer’s disease. Neuroinflammatory changes, including microglial activation and production of inflammatory cytokines, are observed in neurodegenerative diseases and normal aging. The bioenergetic hypothesis advocates for sequential events from metabolic deficits to propagation of neuronal dysfunction, to aging, and to neurodegeneration, while the inflammatory hypothesis supports microglia activation as the driving force for neuroinflammation. Nevertheless, growing evidence suggests that these diverse mechanisms have redox dysregulation as a common denominator and connector. An independent view of the mechanisms underlying brain aging and neurodegeneration is being replaced by one that entails multiple mechanisms coordinating and interacting with each other. This review focuses on the alterations in energy metabolism and inflammatory responses and their connection via redox regulation in normal brain aging and Alzheimer’s disease. Interactions of these systems is reviewed based on basic research and clinical studies.