000130294 001__ 130294
000130294 005__ 20240124152850.0
000130294 0247_ $$2doi$$a10.1016/j.arr.2018.04.006
000130294 0248_ $$2sideral$$a106390
000130294 037__ $$aART-2018-106390
000130294 041__ $$aeng
000130294 100__ $$0(orcid)0000-0003-1508-6516$$aIglesias, E.$$uUniversidad de Zaragoza
000130294 245__ $$aPrenatal exposure to oxidative phosphorylation xenobiotics and late-onset Parkinson disease
000130294 260__ $$c2018
000130294 5203_ $$aLate-onset Parkinson disease is a multifactorial and multietiological disorder, age being one of the factors implicated. Genetic and/or environmental factors, such as pesticides, can also be involved. Up to 80% of dopaminergic neurons of the substantia nigra are lost before motor features of the disorder begin to appear. In humans, these neurons are only formed a few weeks after fertilization. Therefore, prenatal exposure to pesticides or industrial chemicals during crucial steps of brain development might also alter their proliferation and differentiation. Oxidative phosphorylation is one of the metabolic pathways sensitive to environmental toxicants and it is crucial for neuronal differentiation. Many inhibitors of this biochemical pathway, frequently found as persistent organic pollutants, affect dopaminergic neurogenesis, promote the degeneration of these neurons and increase the risk of suffering late-onset Parkinson disease. Here, we discuss how an early, prenatal, exposure to these oxidative phosphorylation xenobiotics might trigger a late-onset, old age, Parkinson disease.
000130294 536__ $$9info:eu-repo/grantAgreement/ES/DGA/B33-17R$$9info:eu-repo/grantAgreement/ES/FIS/PI17-00021$$9info:eu-repo/grantAgreement/ES/FIS/PI17-00166$$9info:eu-repo/grantAgreement/ES/ISCIII/P114-00005
000130294 540__ $$9info:eu-repo/semantics/openAccess$$aAll rights reserved$$uhttp://www.europeana.eu/rights/rr-f/
000130294 590__ $$a10.39$$b2018
000130294 591__ $$aGERIATRICS & GERONTOLOGY$$b2 / 53 = 0.038$$c2018$$dQ1$$eT1
000130294 591__ $$aCELL BIOLOGY$$b18 / 191 = 0.094$$c2018$$dQ1$$eT1
000130294 592__ $$a4.125$$b2018
000130294 593__ $$aAging$$c2018$$dQ1
000130294 593__ $$aBiochemistry$$c2018$$dQ1
000130294 593__ $$aNeurology$$c2018$$dQ1
000130294 593__ $$aMolecular Biology$$c2018$$dQ1
000130294 593__ $$aBiotechnology$$c2018$$dQ1
000130294 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/acceptedVersion
000130294 700__ $$0(orcid)0000-0001-9695-7349$$aPesini, A.$$uUniversidad de Zaragoza
000130294 700__ $$0(orcid)0000-0003-0145-3020$$aGarrido-Pérez, N.$$uUniversidad de Zaragoza
000130294 700__ $$0(orcid)0000-0002-3587-6622$$aMeade, P.$$uUniversidad de Zaragoza
000130294 700__ $$0(orcid)0000-0002-8585-6371$$aBayona-Bafaluy, M.P.$$uUniversidad de Zaragoza
000130294 700__ $$0(orcid)0000-0003-1770-6299$$aMontoya, J.$$uUniversidad de Zaragoza
000130294 700__ $$0(orcid)0000-0002-0269-7337$$aRuiz-Pesini, E.$$uUniversidad de Zaragoza
000130294 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000130294 773__ $$g45 (2018), 24-32$$pAGEING RES REV$$tAgeing Research Reviews$$x1568-1637
000130294 8564_ $$s540010$$uhttps://zaguan.unizar.es/record/130294/files/texto_completo.pdf$$yPostprint
000130294 8564_ $$s2619767$$uhttps://zaguan.unizar.es/record/130294/files/texto_completo.jpg?subformat=icon$$xicon$$yPostprint
000130294 909CO $$ooai:zaguan.unizar.es:130294$$particulos$$pdriver
000130294 951__ $$a2024-01-24-15:00:39
000130294 980__ $$aARTICLE