A recent study in the journal GeroScience investigated how age-related declines in cellular energy, specifically the molecule Guanosine triphosphate (GTP), affect waste clearance in brain cells. Using hippocampal neurons from an Alzheimer's disease (AD) mouse model, researchers found a significant, age-dependent reduction in free GTP levels, which was accelerated in the AD model neurons. This energy deficit was shown to impair critical cellular processes like endocytosis and autophagy, leading to the accumulation of toxic amyloid-beta (Aß) aggregates and increased protein oxidation. Remarkably, the researchers then treated aged neurons for 24 hours with a combination of nicotinamide (a precursor to the energy-related molecule NAD+) and EGCG (a redox modulator found in green tea). This treatment was highly effective, restoring the depleted GTP levels in aged neurons all the way back to the normal, youthful levels seen in healthy, young neurons. This restoration of cellular energy enhanced the clearance of Aß aggregates and improved the viability of aged AD model neurons by 22%.

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#GTP #Autophagy #AlzheimersResearch #Nicotinamide #EGCG

Source: Santana, R. A., McWhirt, J. M., & Brewer, G. J. (2025). Treatment of age-related decreases in GTP levels restores endocytosis and autophagy. GeroScience. https://doi.org/10.1007/s11357-025-01786-4

Guanosine triphosphate, GTP, Alzheimer's disease, neuronal aging, autophagy, endocytosis, bioenergetics, nicotinamide, EGCG, NAD+, Nrf2, 3xTg-AD mouse model, proteostasis, amyloid-beta clearance, Aß aggregates, mitochondrial dysfunction, cellular energy, redox state, Rab7, Arl8b, neuronal viability, protein oxidation, neurodegeneration, in vitro study, hippocampal neurons