Enhanced oxidative stress and inflammation contribute to telomere erosion. Friedreich's ataxia is a neurodegenerative disorder caused by a reduction in frataxin expression that results in mitochondrial dysfunction and oxidative damage. Furthermore, frataxin deficiency induces a strong activation of inflammatory genes and neuronal death. We investigated telomere length in peripheral blood leukocytes of 37 Friedreich's ataxia patients and 36 controls.
Can telomere shortening in human peripheral blood leukocytes serve as a disease biomarker of Friedreich's Ataxia?
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