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                  <mods:namePart>Pedro-Cuesta, Jesus de</mods:namePart>
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                  <mods:namePart>Martínez-Martín, Pablo</mods:namePart>
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                  <mods:namePart>Rábano, Alberto</mods:namePart>
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                  <mods:namePart>Ruiz-Tovar, Maria</mods:namePart>
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                  <mods:namePart>Alcalde-Cabero, Enrique</mods:namePart>
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                  <mods:namePart>Calero, Miguel</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Instituto de Salud Carlos III</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Unión Europea</mods:namePart>
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                  <mods:dateIssued encoding="iso8601">2016</mods:dateIssued>
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               <mods:identifier type="citation">Front Aging Neurosci. 2016 Jun 13;8:138.</mods:identifier>
               <mods:identifier type="doi">10.3389/fnagi.2016.00138</mods:identifier>
               <mods:identifier type="issn">1663-4365</mods:identifier>
               <mods:identifier type="journal">Frontiers in aging neuroscience</mods:identifier>
               <mods:identifier type="pubmedID">27378910</mods:identifier>
               <mods:identifier type="uri">http://hdl.handle.net/20.500.12105/9732</mods:identifier>
               <mods:abstract>BACKGROUND: 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.</mods:abstract>
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                  <mods:languageTerm authority="rfc3066">eng</mods:languageTerm>
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               <mods:subject>
                  <mods:topic>Disease induction vs. transmission in amyloid</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Epidemiological patterns</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Etiology of conformational protein deposits</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Multidisciplinary research overlaps</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Templating underlying risk/progression</mods:topic>
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               <mods:titleInfo>
                  <mods:title>Etiologic Framework for the Study of Neurodegenerative Disorders as Well as Vascular and Metabolic Comorbidities on the Grounds of Shared Epidemiologic and Biologic Features</mods:title>
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