Age-Associated Cellular Decline chart.

The science of AACD is continually evolving. This is a compilation of the most important articles, presentations, scientific papers and clinical studies by top experts in the field.

You can explore the science of AACD, focusing on the topics that interest you most:

Redox Analysis of Human Plasma Allows Separation of Pro-Oxidant Events of Aging from Decline in Antioxidant Defenses

This study characterized age-related changes in the balance between oxidative events and the glutathione antioxidant defense system, as measured in the plasma of healthy adults aged 19-85. These data suggest oxidative events increase throughout adult life, but that the capacity of the glutathione antioxidant system is generally maintained only until age 45 and then declines rapidly.
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The Plasma NAD+ Metabolome is Dysregulated in 'Normal' Aging

Intracellular levels of NAD+ have emerged as a major regulator of mitochondrial metabolism in health and disease. NAD+ (Nicotinamide adenine dinucleotide) is a coenzyme that is essential to turn nutrients (carbohydrates and fat) into energy. This study measured changes in levels of NAD+ in healthy adults and showed that levels of NAD+ decline in older age.
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The Hallmarks of Aging

This publication reviews nine processes within the body that decline with age. These nine hallmarks of aging detail genetic pathways and cellular processes that are impacted and includes sections on mitochondrial dysfunction, genomic instability, telomere attrition, deregulated nutrient sensing and cellular senescence.
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Mitophagy in Neurodegeneration and Aging

Mitophagy is a cellular process that regulates the recycling of damaged and dysfunctional mitochondria. This review summarizes research linking reduced mitophagy to aging and cognitive declines in older adults.
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Oxidation Damage Accumulation Aging Theory (The Novel Role of Glutathione)

This paper reviews how glutathione, a powerful intracellular antioxidant protein that is important for the body’s natural defenses and often deficient in older adults, is central to regulating oxidative stress and combating oxidation damage.
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Mitochondrial Oxidative Capacity and NAD+ Biosynthesis are Reduced in Human Sarcopenia Across Ethnicities

This study showed that mitochondrial dysfunction is one of the strongest markers of sarcopenia (age-related muscle loss) in three distinct ethnic populations. Individuals with sarcopenia exhibited major impairments in energy production and significantly lower NAD+ levels.
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Mitochondrial Function is Impaired in the Skeletal Muscle of Pre-Frail Elderly

This clinical study showed that muscle mitochondrial dysfunction is a hallmark of pre-frailty development and the onset of decline in muscle function in older persons.
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A Free Radical Theory of Frailty

Levels of oxidative stress and oxidative damage due to free radicals within the cells are more closely associated with the onset of frailty in older adults, than with chronological age and lifespan. This publication reviews the results from studies supporting a new Free Radical Theory of Frailty, expanding beyond the classic Free Radical Theory of Aging.
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Mitochondrial Aging and Age-Related Dysfunction of Mitochondria

Mitochondria are mainly responsible for generating cellular energy as ATP. Changes to their function, structure, distribution, and dynamics contribute to cellular aging and age-related declines.
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The Mitochondrial Basis of Aging

This paper reviews the evidence of how mitochondrial dysfunction is a key driver in the aging process. It contributes to cellular senescence (when cells stop replicating/no-longer divide), chronic inflammation, reduced stem cell activity, and general age-related decline.
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The Impact of Age Associated Cellular Decline on Bioenergetics and Functional Impairment

This presentation reviews evidence supporting the importance of better mitochondrial function for healthy aging, and how lifestyle habits like regular physical activity and healthy weight management, can improve cellular energy metabolism – the life-sustaining process that happens within our cells.
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