Tau proteini beynin enerji sistemlerini nasıl bozabilir?

Tau normally supports communication between nerve cells, but abnormal forms of the protein accumulate in disorders such as Alzheimer’s disease. An NIH-funded team investigated how these altered proteins affect mitochondria, the structures that generate cellular energy. Experiments involving flies, mice, human brain tissue and cultured nerve cells showed that phosphorylated tau entered mitochondria and activated reverse electron transport, a process capable of damaging cells. The process then increased tau phosphorylation, producing a harmful feedback loop. When researchers used a compound to interrupt reverse electron transport, motor and memory problems declined in animal models, while cultured human nerve cells became more resistant to stress. The findings identify a possible treatment target rather than an established therapy. The compound has not yet reached clinical trials, so further research is needed to determine whether blocking this pathway can safely benefit people with tau-related diseases.