000130321 001__ 130321 000130321 005__ 20240124152850.0 000130321 0247_ $$2doi$$a10.1016/j.redox.2021.101871 000130321 0248_ $$2sideral$$a122369 000130321 037__ $$aART-2021-122369 000130321 041__ $$aeng 000130321 100__ $$0(orcid)0000-0002-8585-6371$$aBayona-Bafaluy, M.P.$$uUniversidad de Zaragoza 000130321 245__ $$aDown syndrome is an oxidative phosphorylation disorder 000130321 260__ $$c2021 000130321 5060_ $$aAccess copy available to the general public$$fUnrestricted 000130321 5203_ $$aDown syndrome is the most common genomic disorder of intellectual disability and is caused by trisomy of chromosome 21. Several genes in this chromosome repress mitochondrial biogenesis. The goal of this study was to evaluate whether early overexpression of these genes may cause a prenatal impairment of oxidative phosphorylation negatively affecting neurogenesis. Reduction in the mitochondrial energy production and a lower mitochondrial function have been reported in diverse tissues or cell types, and also at any age, including early fetuses, suggesting that a defect in oxidative phosphorylation is an early and general event in Down syndrome individuals. Moreover, many of the medical conditions associated with Down syndrome are also frequently found in patients with oxidative phosphorylation disease. Several drugs that enhance mitochondrial biogenesis are nowadays available and some of them have been already tested in mouse models of Down syndrome restoring neurogenesis and cognitive defects. Because neurogenesis relies on a correct mitochondrial function and critical periods of brain development occur mainly in the prenatal and early neonatal stages, therapeutic approaches intended to improve oxidative phosphorylation should be provided in these periods. 000130321 536__ $$9info:eu-repo/grantAgreement/ES/DGA/B33-17R$$9info:eu-repo/grantAgreement/ES/FIS/PI17-00021$$9info:eu-repo/grantAgreement/ES/FIS/PI17-00166 000130321 540__ $$9info:eu-repo/semantics/openAccess$$aby-nc-nd$$uhttp://creativecommons.org/licenses/by-nc-nd/3.0/es/ 000130321 590__ $$a10.787$$b2021 000130321 591__ $$aBIOCHEMISTRY & MOLECULAR BIOLOGY$$b27 / 297 = 0.091$$c2021$$dQ1$$eT1 000130321 592__ $$a2.191$$b2021 000130321 593__ $$aClinical Biochemistry$$c2021$$dQ1 000130321 593__ $$aBiochemistry$$c2021$$dQ1 000130321 594__ $$a16.4$$b2021 000130321 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion 000130321 700__ $$0(orcid)0000-0003-0145-3020$$aGarrido-Pérez, N.$$uUniversidad de Zaragoza 000130321 700__ $$0(orcid)0000-0002-3587-6622$$aMeade, P.$$uUniversidad de Zaragoza 000130321 700__ $$0(orcid)0000-0003-1508-6516$$aIglesias, E. 000130321 700__ $$0(orcid)0000-0002-1426-3958$$aJiménez-Salvador, I.$$uUniversidad de Zaragoza 000130321 700__ $$0(orcid)0000-0003-1770-6299$$aMontoya, J.$$uUniversidad de Zaragoza 000130321 700__ $$aMartínez-Cué, C. 000130321 700__ $$0(orcid)0000-0002-0269-7337$$aRuiz-Pesini, E.$$uUniversidad de Zaragoza 000130321 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole. 000130321 773__ $$g41 (2021), 101871 [12 pp]$$pRedox biol.$$tRedox Biology$$x2213-2317 000130321 8564_ $$s6284910$$uhttps://zaguan.unizar.es/record/130321/files/texto_completo.pdf$$yVersión publicada 000130321 8564_ $$s2460418$$uhttps://zaguan.unizar.es/record/130321/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada 000130321 909CO $$ooai:zaguan.unizar.es:130321$$particulos$$pdriver 000130321 951__ $$a2024-01-24-15:02:57 000130321 980__ $$aARTICLE