Can Telomere Shortening in Human Peripheral Blood Leukocytes Serve as a Disease Biomarker of Friedreich's Ataxia?
| Autor: | Castaldo I, Vergara P, Pinelli M, Filla A, De Michele G, Cocozza S, Monticelli A. |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: | |
| Zdroj: | Antioxidants & redox signalling (2013). info:cnr-pdr/source/autori:Castaldo I, Vergara P, Pinelli M, Filla A, De Michele G, Cocozza S, Monticelli A./titolo:Can Telomere Shortening in Human Peripheral Blood Leukocytes Serve as a Disease Biomarker of Friedreich's Ataxia?/doi:/rivista:Antioxidants & redox signalling/anno:2013/pagina_da:/pagina_a:/intervallo_pagine:/volume |
| Popis: | 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 (TL) in peripheral blood leukocytes of 37 patients with Friedreich's ataxia and 36 controls. We noted a significant telomere shortening in patients with Friedreich's ataxia compared to healthy controls (p=0.03). We also found a correlation between TL and disease duration (p=0.001). Our observations lead to the hypothesis that the TL of human peripheral blood leukocytes may serve as a biomarker of Friedreich's ataxia that could be used as an outcome measure in clinical trials. Antioxid. Redox Signal. 18, 1303-1306. |
| Databáze: | OpenAIRE |
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