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dc.contributor.authorPedro-Cuesta, Jesus de 
dc.contributor.authorMartinez-Martin, Pablo 
dc.contributor.authorRábano, Alberto
dc.contributor.authorRuiz-Tovar, María 
dc.contributor.authorAlcalde-Cabero, Enrique 
dc.contributor.authorCalero, Miguel
dc.identifier.citationFront Aging Neurosci. 2016 Jun 13;8:138.es_ES
dc.description.abstractBACKGROUND: During the last two decades, protein aggregation at all organismal levels, from viruses to humans, has emerged from a neglected area of protein science to become a central issue in biology and biomedicine. This article constitutes a risk-based review aimed at supporting an etiologic scenario of selected, sporadic, protein-associated, i.e., conformational, neurodegenerative disorders (NDDs), and their vascular- and metabolic-associated ailments. METHODS: A rationale is adopted, to incorporate selected clinical data and results from animal-model research, complementing epidemiologic evidences reported in two prior articles. FINDINGS: Theory is formulated assuming an underlying conformational transmission mechanism, mediated either by horizontal transfer of mammalian genes coding for specific aggregation-prone proteins, or by xeno-templating between bacterial and host proteins. We build a few population-based and experimentally-testable hypotheses focusing on: (1) non-disposable surgical instruments for sporadic Creutzfeldt-Jakob disease (sCJD) and other rapid progressive neurodegenerative dementia (sRPNDd), multiple system atrophy (MSA), and motor neuron disease (MND); and (2) specific bacterial infections such as B. pertussis and E. coli for all forms, but particularly for late-life sporadic conformational, NDDs, type 2 diabetes mellitus (T2DM), and atherosclerosis where natural protein fibrils present in such organisms as a result of adaptation to the human host induce prion-like mechanisms. CONCLUSION: Implications for cohort alignment and experimental animal research are discussed and research lines proposed.es_ES
dc.description.sponsorshipFunding was received from the Consortium for Biomedical Research in Neurodegenerative Diseases (Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas/CIBERNED) as part of the 2014–2015 annual budget of the CIBERNED 509-group, and from the Carlos III Institute of Health (PI12/00045). Mr. Alcalde received support from the ISCIII Field Epidemiology Program during 2014 and 2015. The study was partially supported by a grant from the EU Joint Program—Neurodegenerative Disease Research (JPND—DEMTEST (Spanish Health Research Fund, FIS PI11/03021)). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. No author other than EAC received specific funding for this work.es_ES
dc.publisherFrontiers Mediaes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.subjectdisease induction vs. transmission in amyloides_ES
dc.subjectepidemiological patternses_ES
dc.subjectetiology of conformational protein depositses_ES
dc.subjectmultidisciplinary research overlapses_ES
dc.subjecttemplating underlying risk/progressiones_ES
dc.titleEtiologic Framework for the Study of Neurodegenerative Disorders as Well as Vascular and Metabolic Comorbidities on the Grounds of Shared Epidemiologic and Biologic Featureses_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBERes_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.contributor.funderEuropean Uniones_ES
dc.contributor.funderFondo de Investigaciones Sanitariases_ES
dc.identifier.journalFrontiers in aging neurosciencees_ES
dc.repisalud.centroISCIII::Centro Nacional de Epidemologíaes_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/FIS PI11/03021es_ES

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