| Autor: |
Jimenez-Pacheco A; CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Av. Americo Vespucio s/n, 41092, Seville, Spain.; Department of Medical Biochemistry, Molecular Biology and Immunology, University of Seville Medical School, Seville, Spain., Franco JM; CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Av. Americo Vespucio s/n, 41092, Seville, Spain.; Department of Medical Biochemistry, Molecular Biology and Immunology, University of Seville Medical School, Seville, Spain., Lopez S; CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Av. Americo Vespucio s/n, 41092, Seville, Spain.; Department of Medical Biochemistry, Molecular Biology and Immunology, University of Seville Medical School, Seville, Spain., Gomez-Zumaquero JM; Genomic Unit, Malaga Institute of Biomedical Research (IBIMA), Malaga, Spain., Magdalena Leal-Lasarte M; CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Av. Americo Vespucio s/n, 41092, Seville, Spain., Caballero-Hernandez DE; CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Av. Americo Vespucio s/n, 41092, Seville, Spain.; School of Biological Sciences, Autonomous University of Nuevo Leon (UANL), Nuevo Leon, Mexico., Cejudo-Guillén M; CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Av. Americo Vespucio s/n, 41092, Seville, Spain.; Department of Medical Biochemistry, Molecular Biology and Immunology, University of Seville Medical School, Seville, Spain., Pozo D; CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Av. Americo Vespucio s/n, 41092, Seville, Spain. david.pozo@cabimer.es.; Department of Medical Biochemistry, Molecular Biology and Immunology, University of Seville Medical School, Seville, Spain. david.pozo@cabimer.es. |
| Abstrakt: |
Despite being clinically described 150 years ago, the mechanisms underlying amyotrophic lateral sclerosis (ALS) pathogenesis have not yet been fully understood. Studies in both animal models of ALS and human patients reveal a plethora of alterations such as increased glutamate-mediated excitotoxicity, redox stress, increased apoptosis, defective axonal transport, protein-misfolding events, mitochondrial impairment and sustained unregulated immune responses. Regardless of being sporadic or familiar ALS, the final outcome at the cellular level is the death of upper and lower motor neurons, and once diagnosed, ALS is typically lethal within the next 5 years. There are neither clear biomarkers nor therapeutic or disease-modifying treatments for ALS.Accumulating evidence supports the concept that epigenetic-driven modifications, including altered chromatin remodelling events, RNA editing and non-coding RNA molecules, might shed light into the pathogenic mechanisms underlying sporadic/familiar ALS onset and/or severity to facilitate the identification of effective therapies, early diagnosis and potentially early-stage therapeutic interventions to increase the survival outcome of ALS patients. |
