PBN
PBN (alpha-phenyl-tert-butyl nitrone) is a nitrone compound that has shown anti aging potential in studies, especially for neurodegenerative diseases of stroke and Alzheimer's disease.
Studies have suggested that this neuroprotective effect of some of the nitrone group compounds is mostly not due to the compounds free radical trapping activity, but to the functioning against neuroinflammation.
The compounds seem to lead to cessation of enhanced signal transduction processes associated with neuroinflammatory processes known to be enhanced in several neurodegenerative conditions.
Enhanced neuroinflammatory processes produce higher levels of neurotoxins, which have been found to cause death or dysfunction of neurons.
Therefore, quelling of these processes has been considered to have a beneficial effect in proper neuronal functioning.
In fact, some of the possible antiaging activities of thse nitrones may indeed reside in the ability to quell enhanced production of reactive oxygen species associated with age-related conditions.
Some of the research suggests that the products formed by senescent cells on bystander cells is one of the causes of aging, and that nitrones, by mitigating these processes, have an antiaging activity.
Of the nitrone family compounds, the PBN variety has been the most studied.
In one animal study it was found that older gerbils, that normally exhibit significantly higher errors in a radial arm maze than younger animals, had decreased error levels of down to the level of those observed in younger animals when their diet was supplemented with the compound.
PBN - Studies
Floyd RA, Hensley K, Forster MJ, Kelleher-Anderson JA, Wood PL. Nitrones as neuroprotectants and antiaging drugs. Increasing Healthy Life Span: Conventional Measures And Slowing The Innate Aging Process. Annals of the New York Academy of Sciences 2002, 959: 321-329.
Carney JM Floyd RA. Protection against oxidative damage to CNS by alpha-phenyl-tert-butyl nitrone (PBN) and other spin-trapping agents: a novel series of nonlipid free radical scavengers. J Mol Neurosci (1991) 3(1):47-57.
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