Cognitive reserve and lifestyle: moving towards preclinical Alzheimer’s disease
Identifieur interne : 000100 ( Pmc/Curation ); précédent : 000099; suivant : 000101Cognitive reserve and lifestyle: moving towards preclinical Alzheimer’s disease
Auteurs : Eider M. Arenaza-Urquijo [France] ; Miranka Wirth [France] ; Gaël Chételat [France]Source :
- Frontiers in Aging Neuroscience [ 1663-4365 ] ; 2015.
Abstract
The large majority of neuroimaging studies in Alzheimer’s disease (AD) patients have supported the idea that lifestyle factors may protect against the clinical manifestations of AD rather than influence AD neuropathological processes (the cognitive reserve hypothesis). This evidence argues in favor of the hypothesis that lifestyle factors act as moderators between AD pathology and cognition, i.e., through indirect compensatory mechanisms. In this review, we identify emerging evidence in cognitively normal older adults that relate lifestyle factors to established AD neuroimaging biomarkers. While some of these investigations are in agreement with the compensatory view of cognitive reserve, other studies have revealed new clues on the neural mechanisms underlying beneficial effects of lifestyle factors on the brain. Specifically, they provide novel evidence suggesting direct effects of lifestyle factors on AD neuropathological processes. We propose a tentative theoretical model where lifestyle factors may act via direct neuroprotective and/or indirect compensatory mechanisms. Importantly, we suggest that neuroprotective mechanisms may have a major role during early stages and compensatory mechanisms in later stages of the disease. In the absence of an effective treatment for AD and considering the potential of lifestyle factors in AD prevention, understanding the neural mechanisms underlying lifestyle effects on the brain seems crucial. We hope to provide an integrative view that may help to better understand the complex effects of lifestyle factors on AD neuropathological processes, starting from the preclinical stage.
Url:
DOI: 10.3389/fnagi.2015.00134
PubMed: 26321944
PubMed Central: 4530312
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This evidence argues in favor of the hypothesis that lifestyle factors act as moderators between AD pathology and cognition, i.e., through indirect compensatory mechanisms. In this review, we identify emerging evidence in cognitively normal older adults that relate lifestyle factors to established AD neuroimaging biomarkers. While some of these investigations are in agreement with the compensatory view of cognitive reserve, other studies have revealed new clues on the neural mechanisms underlying beneficial effects of lifestyle factors on the brain. Specifically, they provide novel evidence suggesting direct effects of lifestyle factors on AD neuropathological processes. We propose a tentative theoretical model where lifestyle factors may act via direct neuroprotective and/or indirect compensatory mechanisms. Importantly, we suggest that neuroprotective mechanisms may have a major role during early stages and compensatory mechanisms in later stages of the disease. In the absence of an effective treatment for AD and considering the potential of lifestyle factors in AD prevention, understanding the neural mechanisms underlying lifestyle effects on the brain seems crucial. We hope to provide an integrative view that may help to better understand the complex effects of lifestyle factors on AD neuropathological processes, starting from the preclinical stage.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Alexander, G E" uniqKey="Alexander G">G. E. Alexander</name></author><author><name sortKey="Furey, M L" uniqKey="Furey M">M. L. Furey</name></author><author><name sortKey="Grady, C L" uniqKey="Grady C">C. L. Grady</name></author><author><name sortKey="Pietrini, P" uniqKey="Pietrini P">P. Pietrini</name></author><author><name sortKey="Brady, D R" uniqKey="Brady D">D. R. Brady</name></author><author><name sortKey="Mentis, M J" uniqKey="Mentis M">M. J. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Aging Neurosci</journal-id><journal-id journal-id-type="iso-abbrev">Front Aging Neurosci</journal-id><journal-id journal-id-type="publisher-id">Front. Aging Neurosci.</journal-id><journal-title-group><journal-title>Frontiers in Aging Neuroscience</journal-title></journal-title-group><issn pub-type="epub">1663-4365</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26321944</article-id><article-id pub-id-type="pmc">4530312</article-id><article-id pub-id-type="doi">10.3389/fnagi.2015.00134</article-id><article-categories><subj-group subj-group-type="heading"><subject>Neuroscience</subject><subj-group><subject>Review</subject></subj-group></subj-group></article-categories><title-group><article-title>Cognitive reserve and lifestyle: moving towards preclinical Alzheimer’s disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Arenaza-Urquijo</surname><given-names>Eider M.</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="aff" rid="aff4"><sup>4</sup></xref><xref ref-type="author-notes" rid="fn001"><sup>*</sup></xref><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/48757"></uri></contrib><contrib contrib-type="author"><name><surname>Wirth</surname><given-names>Miranka</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="aff" rid="aff4"><sup>4</sup></xref><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/222655"></uri></contrib><contrib contrib-type="author"><name><surname>Chételat</surname><given-names>Gaël</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="aff" rid="aff4"><sup>4</sup></xref><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/74040"></uri></contrib></contrib-group><aff id="aff1"><sup>1</sup><institution>INSERM, U1077</institution><country>Caen, France</country></aff><aff id="aff2"><sup>2</sup><institution>Université de Caen Basse-Normandie, UMR-S1077</institution><country>Caen, France</country></aff><aff id="aff3"><sup>3</sup><institution>Ecole Pratique des Hautes Etudes, UMR-S1077</institution><country>Caen, France</country></aff><aff id="aff4"><sup>4</sup><institution>CHU de Caen, U1077</institution><country>Caen, France</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Simone Rossi, Azienda Ospedalira Universitaria Senese, Italy</p></fn><fn fn-type="edited-by"><p>Reviewed by: Federica Agosta, Vita-Salute San Raffaele University, Italy; Paolo M. Rossini, IRCCS San Raffaele Pisana and Università Cattolica del Sacro Cuore-Roma, Italy</p></fn><corresp id="fn001">*Correspondence: Eider M. Arenaza-Urquijo, Neuropsychology and Functional Neuroanatomy of the Human Memory, INSERM, U1077, Université de Caen Basse-Normandie, UMR-S1077, Ecole Pratique des Hautes Etudes, UMR-S1077, Bd. H. Becquerel, BP 5229, F-14074 Caen, France <email xlink:type="simple">arenaza@cyceron.fr</email></corresp></author-notes><pub-date pub-type="epub"><day>10</day><month>8</month><year>2015</year></pub-date><pub-date pub-type="collection"><year>2015</year></pub-date><volume>7</volume><elocation-id>134</elocation-id><history><date date-type="received"><day>12</day><month>3</month><year>2015</year></date><date date-type="accepted"><day>29</day><month>6</month><year>2015</year></date></history><permissions><copyright-statement>Copyright © 2015 Arenaza-Urquijo, Wirth and Chételat.</copyright-statement><copyright-year>2015</copyright-year><copyright-holder>Arenaza-Urquijo, Wirth and Chételat</copyright-holder><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p></license></permissions><abstract><p>The large majority of neuroimaging studies in Alzheimer’s disease (AD) patients have supported the idea that lifestyle factors may protect against the clinical manifestations of AD rather than influence AD neuropathological processes (the cognitive reserve hypothesis). This evidence argues in favor of the hypothesis that lifestyle factors act as moderators between AD pathology and cognition, i.e., through indirect compensatory mechanisms. In this review, we identify emerging evidence in cognitively normal older adults that relate lifestyle factors to established AD neuroimaging biomarkers. While some of these investigations are in agreement with the compensatory view of cognitive reserve, other studies have revealed new clues on the neural mechanisms underlying beneficial effects of lifestyle factors on the brain. Specifically, they provide novel evidence suggesting direct effects of lifestyle factors on AD neuropathological processes. We propose a tentative theoretical model where lifestyle factors may act via direct neuroprotective and/or indirect compensatory mechanisms. Importantly, we suggest that neuroprotective mechanisms may have a major role during early stages and compensatory mechanisms in later stages of the disease. In the absence of an effective treatment for AD and considering the potential of lifestyle factors in AD prevention, understanding the neural mechanisms underlying lifestyle effects on the brain seems crucial. We hope to provide an integrative view that may help to better understand the complex effects of lifestyle factors on AD neuropathological processes, starting from the preclinical stage.</p></abstract><kwd-group><kwd>cognitive reserve</kwd><kwd>brain reserve</kwd><kwd>neuroimaging</kwd><kwd>Alzheimer’s disease</kwd><kwd>amyloid</kwd><kwd>preclinical Alzheimer’s disease</kwd><kwd>compensation</kwd><kwd>neuroprotection</kwd></kwd-group><counts><fig-count count="4"></fig-count><table-count count="0"></table-count><equation-count count="0"></equation-count><ref-count count="96"></ref-count><page-count count="12"></page-count><word-count count="9853"></word-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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