Scientific Articles

The following peer-reviewed articles discuss multiple aspects of microbiology and pre-clinical experimentation related to aging. At least one author of each article is a member of Juvenon's Scientific Advisory Board. The articles are listed here to summarize the depth and breadth of scientific inquiry that stands behind Juvenon, Inc.

The articles are not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The label should be consulted for intended uses and appropriate directions for use of the Juvenon product.

	Increasing longevity by tuning up metabolism
	Mineral and vitamin deficiencies can accelerate the mitochondrial decay of aging.
	Delaying the mitochondrial decay of aging with acetylcarnitine.
	Mitochondrial decay, a major cause of aging, can be delayed.
	Feeding acetyl-L-carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress.
	Age-associated mitochondrial oxidative decay: Improvement of carnitine acetyltransferase substrate-binding affinity and activity in brain by feeding old rats acetly-l-carnitine and/or R-alpha-lipoic acid.
	Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: Partial reversal by feeding acetyl-L-carnitine and/or R-alpha-lipoic acid.
	Acetyl L-carnitine fed to old rats partially restores mitochondrial function and ambulatory activity.
	Oxidative damage and mitochondrial decay in aging.
	The Free Radical Theory of Aging Matures.
	Comparison of the effects of L-carnitine and acetyl-L-carnitine on carnitine levels, ambulatory activity, and oxidative stress biomarkers in the brain of old rats.
	R-alpha-Lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage and increased metabolic rate.
	Age-associated decline in ascorbic acid concentration, recycling, and biosynthesis in rat hepatocytes - reversal with (R)-a lipoic acid supplementation.
	R-alpha-Lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate.
	Mitochondrial decay in hepatocytes from old rats: Membrane potential declines, heterogeneity and oxidants increase.
	R-alpha lipoic acid reverses the age-related loss in redox status in post-mitotic tissues: evidence for increased cysteine requirement for GSH status.
	Decline in transcriptional activity of Nrf2 causes age-related loss of glutathione synthesis, which is reversible with lipoic acid.