Taurine is a dietary amino acid. Circulating levels in the bloodstream decline with age, but can be restored by supplementation. Taurine supplementation has been shown to produce improved health and modest life extension in mice, and may act to improve protective cellular antioxidant mechanisms, though other mechanisms are likely involved. Human trials have been less promising, but largely predated modern approaches to measuring biological age, and may have been looking at overly specific measurable biomarkers of oxidative metabolism. Given that taurine is safe and cheap, it is an interesting intervention for self-experimenters, even though we shouldn't expect the effects on health and life span to be large in humans.
Aging-related biochemical changes in nerve cells lead to dysfunctional synapses and disrupted neuronal circuits, ultimately affecting vital processes such as brain plasticity, learning, and memory. The imbalance between excitation and inhibition in synaptic function during aging contributes to cognitive impairment, emphasizing the importance of compensatory mechanisms. Fear conditioning-related plasticity of the somatosensory barrel cortex, relying on the proper functioning and extensive up regulation of the GABAergic system, in particular interneurons containing somatostatin, is compromised in aging (one-year-old) mice. The present research explores two potential interventions, taurine supplementation, and environmental enrichment, revealing their effectiveness in supporting learning-induced plasticity in the aging mouse brain. They do not act through a mechanism normalizing the Glutamate/GABA balance that is disrupted in aging. Still, they allow for increased somatostatin levels, an effect observed in young animals after learning. These findings highlight the potential of lifestyle interventions and diet supplementation to mitigate age-related cognitive decline by promoting experience-dependent plasticity.
Link: https://doi.org/10.1038/s41598-024-70261-5
