<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-05-20T23:32:33Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/9732" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/9732</identifier><datestamp>2025-06-13T10:00:54Z</datestamp><setSpec>com_20.500.12105_2052</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19608</setSpec><setSpec>col_20.500.12105_19617</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Pedro-Cuesta, Jesus de</subfield>
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      <subfield code="a">Martínez-Martín, Pablo</subfield>
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      <subfield code="a">Rábano, Alberto</subfield>
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      <subfield code="a">Ruiz-Tovar, Maria</subfield>
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      <subfield code="a">Alcalde-Cabero, Enrique</subfield>
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      <subfield code="a">Calero, Miguel</subfield>
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      <subfield code="c">2016</subfield>
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      <subfield code="a">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.</subfield>
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      <subfield code="a">Front Aging Neurosci. 2016 Jun 13;8:138.</subfield>
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      <subfield code="a">10.3389/fnagi.2016.00138</subfield>
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      <subfield code="a">1663-4365</subfield>
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      <subfield code="a">Frontiers in aging neuroscience</subfield>
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      <subfield code="a">27378910</subfield>
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   <datafield ind1="8" ind2=" " tag="024">
      <subfield code="a">http://hdl.handle.net/20.500.12105/9732</subfield>
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   <datafield tag="653" ind2=" " ind1=" ">
      <subfield code="a">Disease induction vs. transmission in amyloid</subfield>
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   <datafield tag="653" ind2=" " ind1=" ">
      <subfield code="a">Epidemiological patterns</subfield>
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   <datafield tag="653" ind2=" " ind1=" ">
      <subfield code="a">Etiology of conformational protein deposits</subfield>
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      <subfield code="a">Multidisciplinary research overlaps</subfield>
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      <subfield code="a">Templating underlying risk/progression</subfield>
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   <datafield ind2="0" ind1="0" tag="245">
      <subfield code="a">Etiologic Framework for the Study of Neurodegenerative Disorders as Well as Vascular and Metabolic Comorbidities on the Grounds of Shared Epidemiologic and Biologic Features</subfield>
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