Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease
Abstract Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited...
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| creator | Brown, Belinda M Sohrabi, Hamid R Taddei, Kevin Gardener, Samantha L Rainey-Smith, Stephanie R Peiffer, Jeremiah J Xiong, Chengjie Fagan, Anne M Benzinger, Tammie Buckles, Virginia Erickson, Kirk I Clarnette, Roger Shah, Tejal Masters, Colin L Weiner, Michael Cairns, Nigel Rossor, Martin Graff-Radford, Neill R Salloway, Stephen Vöglein, Jonathan Laske, Christoph Noble, James Schofield, Peter R Bateman, Randall J Morris, John C Martins, Ralph N |
| description | Abstract Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42 , or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers. |
| doi_str_mv | 10.1016/j.jalz.2017.03.008 |
| format | Article |
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Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42 , or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.</description><identifier>ISSN: 1552-5260</identifier><identifier>ISSN: 1552-5279</identifier><identifier>EISSN: 1552-5279</identifier><identifier>DOI: 10.1016/j.jalz.2017.03.008</identifier><identifier>PMID: 28501451</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Alzheimer Disease - diagnostic imaging ; Alzheimer Disease - genetics ; Alzheimer Disease - metabolism ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Amyloid - metabolism ; Amyloid beta-Peptides - cerebrospinal fluid ; Amyloid beta-Protein Precursor - genetics ; Amyloid β ; Aniline Compounds ; Apolipoproteins E - genetics ; Brain - diagnostic imaging ; Brain - metabolism ; Cohort Studies ; Cross-Sectional Studies ; Dementia ; Exercise - physiology ; Female ; Genetics ; Genotype ; Humans ; Linear Models ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Mutation - genetics ; Neurology ; Peptide Fragments - cerebrospinal fluid ; Physical activity ; Positron-Emission Tomography ; Presenilin-1 - genetics ; Presenilin-2 - genetics ; Surveys and Questionnaires ; Tau ; tau Proteins - cerebrospinal fluid ; Thiazoles</subject><ispartof>Alzheimer's & dementia, 2017-11, Vol.13 (11), p.1197-1206</ispartof><rights>the Alzheimer's Association</rights><rights>2017 the Alzheimer's Association</rights><rights>2017 The Alzheimer's Association</rights><rights>Copyright © 2017 the Alzheimer's Association. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5138-b89c6ea4c7129554337186234d83c6493a0b92207190b025bce877cb41d1d4b83</citedby><cites>FETCH-LOGICAL-c5138-b89c6ea4c7129554337186234d83c6493a0b92207190b025bce877cb41d1d4b83</cites><orcidid>0000-0001-7927-2540</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.jalz.2017.03.008$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1016%2Fj.jalz.2017.03.008$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28501451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brown, Belinda M</creatorcontrib><creatorcontrib>Sohrabi, Hamid R</creatorcontrib><creatorcontrib>Taddei, Kevin</creatorcontrib><creatorcontrib>Gardener, Samantha L</creatorcontrib><creatorcontrib>Rainey-Smith, Stephanie R</creatorcontrib><creatorcontrib>Peiffer, Jeremiah J</creatorcontrib><creatorcontrib>Xiong, Chengjie</creatorcontrib><creatorcontrib>Fagan, Anne M</creatorcontrib><creatorcontrib>Benzinger, Tammie</creatorcontrib><creatorcontrib>Buckles, Virginia</creatorcontrib><creatorcontrib>Erickson, Kirk I</creatorcontrib><creatorcontrib>Clarnette, Roger</creatorcontrib><creatorcontrib>Shah, Tejal</creatorcontrib><creatorcontrib>Masters, Colin L</creatorcontrib><creatorcontrib>Weiner, Michael</creatorcontrib><creatorcontrib>Cairns, Nigel</creatorcontrib><creatorcontrib>Rossor, Martin</creatorcontrib><creatorcontrib>Graff-Radford, Neill R</creatorcontrib><creatorcontrib>Salloway, Stephen</creatorcontrib><creatorcontrib>Vöglein, Jonathan</creatorcontrib><creatorcontrib>Laske, Christoph</creatorcontrib><creatorcontrib>Noble, James</creatorcontrib><creatorcontrib>Schofield, Peter R</creatorcontrib><creatorcontrib>Bateman, Randall J</creatorcontrib><creatorcontrib>Morris, John C</creatorcontrib><creatorcontrib>Martins, Ralph N</creatorcontrib><creatorcontrib>The Dominantly Inherited Alzheimer Network</creatorcontrib><creatorcontrib>Dominantly Inherited Alzheimer Network</creatorcontrib><title>Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease</title><title>Alzheimer's & dementia</title><addtitle>Alzheimers Dement</addtitle><description>Abstract Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42 , or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.</description><subject>Adult</subject><subject>Alzheimer Disease - diagnostic imaging</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid - metabolism</subject><subject>Amyloid beta-Peptides - cerebrospinal fluid</subject><subject>Amyloid beta-Protein Precursor - genetics</subject><subject>Amyloid β</subject><subject>Aniline Compounds</subject><subject>Apolipoproteins E - genetics</subject><subject>Brain - diagnostic imaging</subject><subject>Brain - metabolism</subject><subject>Cohort Studies</subject><subject>Cross-Sectional Studies</subject><subject>Dementia</subject><subject>Exercise - physiology</subject><subject>Female</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Humans</subject><subject>Linear Models</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation - genetics</subject><subject>Neurology</subject><subject>Peptide Fragments - cerebrospinal fluid</subject><subject>Physical activity</subject><subject>Positron-Emission Tomography</subject><subject>Presenilin-1 - genetics</subject><subject>Presenilin-2 - genetics</subject><subject>Surveys and Questionnaires</subject><subject>Tau</subject><subject>tau Proteins - cerebrospinal fluid</subject><subject>Thiazoles</subject><issn>1552-5260</issn><issn>1552-5279</issn><issn>1552-5279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUstu1TAQjRCIlsIPsEDeweaG8SsPCSFdVdCHrsQC2LCxHHuq-uLEFztpSfl5HKV0wQKxsUejc87MnJmieEmhpECrt_tyr_1dyYDWJfASoHlUHFMp2Uayun38EFdwVDxLaQ8goKHyaXHEGglUSHpc_DrXnRsn7Qn-xGhcQuLxBn0iOiLRKQXj9IiW3LrxmhiM2MUM1v3sg7PEB22JG8ghYpr7wxh6PTpD9DSGlGNPbOjdoIeRbP3dNboe4-tEbC6jEz4vnlxpn_DF_X9SfP344cvp-Wb36ezidLvbGEl5s-ma1lSohakpa6UUnNe0qRgXtuGmEi3X0LWMQU1b6IDJzmBT16YT1FIruoafFG9W3UMMPyZMo-pdMui9HjBMSdGmbSkVIESGshVqYkgp4pU6RNfrOCsKajFd7dViulpMV8BVNj2TXt3rT12P9oHyx-UM2K6AW-dx_g9Jtd19u7zMz5IDvhZ5t2rk3eCNw6iScTgYtC6iGZUN7t89vv-LbrwbnNH-O86Y9mGKQ96BoioxBerzcjrL5dCa5xlqwX8DPDm8xw</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>Brown, Belinda M</creator><creator>Sohrabi, Hamid R</creator><creator>Taddei, Kevin</creator><creator>Gardener, Samantha L</creator><creator>Rainey-Smith, Stephanie R</creator><creator>Peiffer, Jeremiah J</creator><creator>Xiong, Chengjie</creator><creator>Fagan, Anne M</creator><creator>Benzinger, Tammie</creator><creator>Buckles, Virginia</creator><creator>Erickson, Kirk I</creator><creator>Clarnette, Roger</creator><creator>Shah, Tejal</creator><creator>Masters, Colin L</creator><creator>Weiner, Michael</creator><creator>Cairns, Nigel</creator><creator>Rossor, Martin</creator><creator>Graff-Radford, Neill R</creator><creator>Salloway, Stephen</creator><creator>Vöglein, Jonathan</creator><creator>Laske, Christoph</creator><creator>Noble, James</creator><creator>Schofield, Peter R</creator><creator>Bateman, Randall J</creator><creator>Morris, John C</creator><creator>Martins, Ralph N</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7927-2540</orcidid></search><sort><creationdate>201711</creationdate><title>Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease</title><author>Brown, Belinda M ; Sohrabi, Hamid R ; Taddei, Kevin ; Gardener, Samantha L ; Rainey-Smith, Stephanie R ; Peiffer, Jeremiah J ; Xiong, Chengjie ; Fagan, Anne M ; Benzinger, Tammie ; Buckles, Virginia ; Erickson, Kirk I ; Clarnette, Roger ; Shah, Tejal ; Masters, Colin L ; Weiner, Michael ; Cairns, Nigel ; Rossor, Martin ; Graff-Radford, Neill R ; Salloway, Stephen ; Vöglein, Jonathan ; Laske, Christoph ; Noble, James ; Schofield, Peter R ; Bateman, Randall J ; Morris, John C ; Martins, Ralph N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5138-b89c6ea4c7129554337186234d83c6493a0b92207190b025bce877cb41d1d4b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Alzheimer Disease - diagnostic imaging</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid - metabolism</topic><topic>Amyloid beta-Peptides - cerebrospinal fluid</topic><topic>Amyloid beta-Protein Precursor - genetics</topic><topic>Amyloid β</topic><topic>Aniline Compounds</topic><topic>Apolipoproteins E - genetics</topic><topic>Brain - diagnostic imaging</topic><topic>Brain - metabolism</topic><topic>Cohort Studies</topic><topic>Cross-Sectional Studies</topic><topic>Dementia</topic><topic>Exercise - physiology</topic><topic>Female</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Humans</topic><topic>Linear Models</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation - genetics</topic><topic>Neurology</topic><topic>Peptide Fragments - cerebrospinal fluid</topic><topic>Physical activity</topic><topic>Positron-Emission Tomography</topic><topic>Presenilin-1 - genetics</topic><topic>Presenilin-2 - genetics</topic><topic>Surveys and Questionnaires</topic><topic>Tau</topic><topic>tau Proteins - cerebrospinal fluid</topic><topic>Thiazoles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brown, Belinda M</creatorcontrib><creatorcontrib>Sohrabi, Hamid R</creatorcontrib><creatorcontrib>Taddei, Kevin</creatorcontrib><creatorcontrib>Gardener, Samantha L</creatorcontrib><creatorcontrib>Rainey-Smith, Stephanie R</creatorcontrib><creatorcontrib>Peiffer, Jeremiah J</creatorcontrib><creatorcontrib>Xiong, Chengjie</creatorcontrib><creatorcontrib>Fagan, Anne M</creatorcontrib><creatorcontrib>Benzinger, Tammie</creatorcontrib><creatorcontrib>Buckles, Virginia</creatorcontrib><creatorcontrib>Erickson, Kirk I</creatorcontrib><creatorcontrib>Clarnette, Roger</creatorcontrib><creatorcontrib>Shah, Tejal</creatorcontrib><creatorcontrib>Masters, Colin L</creatorcontrib><creatorcontrib>Weiner, Michael</creatorcontrib><creatorcontrib>Cairns, Nigel</creatorcontrib><creatorcontrib>Rossor, Martin</creatorcontrib><creatorcontrib>Graff-Radford, Neill R</creatorcontrib><creatorcontrib>Salloway, Stephen</creatorcontrib><creatorcontrib>Vöglein, Jonathan</creatorcontrib><creatorcontrib>Laske, Christoph</creatorcontrib><creatorcontrib>Noble, James</creatorcontrib><creatorcontrib>Schofield, Peter R</creatorcontrib><creatorcontrib>Bateman, Randall J</creatorcontrib><creatorcontrib>Morris, John C</creatorcontrib><creatorcontrib>Martins, Ralph N</creatorcontrib><creatorcontrib>The Dominantly Inherited Alzheimer Network</creatorcontrib><creatorcontrib>Dominantly Inherited Alzheimer Network</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Alzheimer's & dementia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, Belinda M</au><au>Sohrabi, Hamid R</au><au>Taddei, Kevin</au><au>Gardener, Samantha L</au><au>Rainey-Smith, Stephanie R</au><au>Peiffer, Jeremiah J</au><au>Xiong, Chengjie</au><au>Fagan, Anne M</au><au>Benzinger, Tammie</au><au>Buckles, Virginia</au><au>Erickson, Kirk I</au><au>Clarnette, Roger</au><au>Shah, Tejal</au><au>Masters, Colin L</au><au>Weiner, Michael</au><au>Cairns, Nigel</au><au>Rossor, Martin</au><au>Graff-Radford, Neill R</au><au>Salloway, Stephen</au><au>Vöglein, Jonathan</au><au>Laske, Christoph</au><au>Noble, James</au><au>Schofield, Peter R</au><au>Bateman, Randall J</au><au>Morris, John C</au><au>Martins, Ralph N</au><aucorp>The Dominantly Inherited Alzheimer Network</aucorp><aucorp>Dominantly Inherited Alzheimer Network</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease</atitle><jtitle>Alzheimer's & dementia</jtitle><addtitle>Alzheimers Dement</addtitle><date>2017-11</date><risdate>2017</risdate><volume>13</volume><issue>11</issue><spage>1197</spage><epage>1206</epage><pages>1197-1206</pages><issn>1552-5260</issn><issn>1552-5279</issn><eissn>1552-5279</eissn><abstract>Abstract Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42 , or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28501451</pmid><doi>10.1016/j.jalz.2017.03.008</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-7927-2540</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Alzheimer Disease - diagnostic imaging Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Alzheimer's disease Amyloid - metabolism Amyloid beta-Peptides - cerebrospinal fluid Amyloid beta-Protein Precursor - genetics Amyloid β Aniline Compounds Apolipoproteins E - genetics Brain - diagnostic imaging Brain - metabolism Cohort Studies Cross-Sectional Studies Dementia Exercise - physiology Female Genetics Genotype Humans Linear Models Magnetic Resonance Imaging Male Middle Aged Mutation - genetics Neurology Peptide Fragments - cerebrospinal fluid Physical activity Positron-Emission Tomography Presenilin-1 - genetics Presenilin-2 - genetics Surveys and Questionnaires Tau tau Proteins - cerebrospinal fluid Thiazoles |
| title | Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease |
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