Abnormal brain structure mediates the association between ApoE4 and slow gait among patients with pathological cognitive impairment: Results from the Ontario Neurodegenerative Research Initiative
Background Presence of at least one copy of the polymorphic apolipoprotein E ε4 allele (ApoE4) increases the risk of impairments of gait performance, particularly in elderly individuals with cognitive impairment or at risk of dementia; however, its underlying neural mechanism are unclear. This study...
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| Veröffentlicht in: | Alzheimer's & dementia 2020-12, Vol.16, p.n/a |
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| creator | Sakurai, Ryota Faria‐Pieruccini, Frederico Dilliott, Allison Ann Hegele, Robert Tartaglia, Carmela McLaughlin, Paula Binns, Malcolm Blue, Korbin Cornish, Ben Sunderland, Kelly M Beaton, Derek Haddad, Seyyed M.H. Tan, Brian Swartz, Richard H. Kwan, Donna Masellis, Mario Ramirez, Joel Roberts, Angela C Black, Sandra E. Symons, Sean Strother, Stephen C Borrie, Michael Pasternak, Stephen H. Freedman, Morris Bartha, Robert Lang, Anthony Munoz, Douglas McIlroy, Bill Montero‐Odasso, Manuel |
| description | Background
Presence of at least one copy of the polymorphic apolipoprotein E ε4 allele (ApoE4) increases the risk of impairments of gait performance, particularly in elderly individuals with cognitive impairment or at risk of dementia; however, its underlying neural mechanism are unclear. This study examined the association among ApoE4, gait performance, and brain structural changes among elderly individuals with cognitive impairment.
Method
Overall, 269 older adults with Alzheimer’s disease, cerebrovascular disease with and without cognitive impairment, and mild cognitive impairment were included from the Ontario Neurodegenerative Disease Research Initiative, who were either ApoE4 carriers (n=98) or non‐ApoE4 (n=171) carriers. Gait speed was measured using an electronic walkway; speed |
| doi_str_mv | 10.1002/alz.044540 |
| format | Article |
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Presence of at least one copy of the polymorphic apolipoprotein E ε4 allele (ApoE4) increases the risk of impairments of gait performance, particularly in elderly individuals with cognitive impairment or at risk of dementia; however, its underlying neural mechanism are unclear. This study examined the association among ApoE4, gait performance, and brain structural changes among elderly individuals with cognitive impairment.
Method
Overall, 269 older adults with Alzheimer’s disease, cerebrovascular disease with and without cognitive impairment, and mild cognitive impairment were included from the Ontario Neurodegenerative Disease Research Initiative, who were either ApoE4 carriers (n=98) or non‐ApoE4 (n=171) carriers. Gait speed was measured using an electronic walkway; speed <1 m/s was defined as slow gait. Participants were stratified into four groups according to the presence of at least one copy of ApoE4 and slow gait. Region of interest volumes were derived by automated segmentation using a 3.0T magnetic resonance imaging system.
Result
Among ApoE4 carriers, 65 (24.2%) participants had slow gait. ApoE4 carriers with slow gait showed significantly higher burden of white matter hyperintensities compared with ApoE4 carriers without slow gait. Moreover, they had significantly lower hippocampal volume and greater total sulcal cerebrospinal fluid volume compared with non‐ApoE4 carriers with slow gait. These differences remained significant despite controlling for covariates (e.g., demographic and clinical characteristics, including participant type).
Conclusion
Our results suggest that brain structural changes, attributable to Alzheimer’s pathology, may mediate the association between ApoE4 and slow gait among elderly individuals with pathological cognitive impairment.</description><identifier>ISSN: 1552-5260</identifier><identifier>EISSN: 1552-5279</identifier><identifier>DOI: 10.1002/alz.044540</identifier><language>eng</language><ispartof>Alzheimer's & dementia, 2020-12, Vol.16, p.n/a</ispartof><rights>2020 the Alzheimer's Association</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Falz.044540$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Falz.044540$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids></links><search><creatorcontrib>Sakurai, Ryota</creatorcontrib><creatorcontrib>Faria‐Pieruccini, Frederico</creatorcontrib><creatorcontrib>Dilliott, Allison Ann</creatorcontrib><creatorcontrib>Hegele, Robert</creatorcontrib><creatorcontrib>Tartaglia, Carmela</creatorcontrib><creatorcontrib>McLaughlin, Paula</creatorcontrib><creatorcontrib>Binns, Malcolm</creatorcontrib><creatorcontrib>Blue, Korbin</creatorcontrib><creatorcontrib>Cornish, Ben</creatorcontrib><creatorcontrib>Sunderland, Kelly M</creatorcontrib><creatorcontrib>Beaton, Derek</creatorcontrib><creatorcontrib>Haddad, Seyyed M.H.</creatorcontrib><creatorcontrib>Tan, Brian</creatorcontrib><creatorcontrib>Swartz, Richard H.</creatorcontrib><creatorcontrib>Kwan, Donna</creatorcontrib><creatorcontrib>Masellis, Mario</creatorcontrib><creatorcontrib>Ramirez, Joel</creatorcontrib><creatorcontrib>Roberts, Angela C</creatorcontrib><creatorcontrib>Black, Sandra E.</creatorcontrib><creatorcontrib>Symons, Sean</creatorcontrib><creatorcontrib>Strother, Stephen C</creatorcontrib><creatorcontrib>Borrie, Michael</creatorcontrib><creatorcontrib>Pasternak, Stephen H.</creatorcontrib><creatorcontrib>Freedman, Morris</creatorcontrib><creatorcontrib>Bartha, Robert</creatorcontrib><creatorcontrib>Lang, Anthony</creatorcontrib><creatorcontrib>Munoz, Douglas</creatorcontrib><creatorcontrib>McIlroy, Bill</creatorcontrib><creatorcontrib>Montero‐Odasso, Manuel</creatorcontrib><title>Abnormal brain structure mediates the association between ApoE4 and slow gait among patients with pathological cognitive impairment: Results from the Ontario Neurodegenerative Research Initiative</title><title>Alzheimer's & dementia</title><description>Background
Presence of at least one copy of the polymorphic apolipoprotein E ε4 allele (ApoE4) increases the risk of impairments of gait performance, particularly in elderly individuals with cognitive impairment or at risk of dementia; however, its underlying neural mechanism are unclear. This study examined the association among ApoE4, gait performance, and brain structural changes among elderly individuals with cognitive impairment.
Method
Overall, 269 older adults with Alzheimer’s disease, cerebrovascular disease with and without cognitive impairment, and mild cognitive impairment were included from the Ontario Neurodegenerative Disease Research Initiative, who were either ApoE4 carriers (n=98) or non‐ApoE4 (n=171) carriers. Gait speed was measured using an electronic walkway; speed <1 m/s was defined as slow gait. Participants were stratified into four groups according to the presence of at least one copy of ApoE4 and slow gait. Region of interest volumes were derived by automated segmentation using a 3.0T magnetic resonance imaging system.
Result
Among ApoE4 carriers, 65 (24.2%) participants had slow gait. ApoE4 carriers with slow gait showed significantly higher burden of white matter hyperintensities compared with ApoE4 carriers without slow gait. Moreover, they had significantly lower hippocampal volume and greater total sulcal cerebrospinal fluid volume compared with non‐ApoE4 carriers with slow gait. These differences remained significant despite controlling for covariates (e.g., demographic and clinical characteristics, including participant type).
Conclusion
Our results suggest that brain structural changes, attributable to Alzheimer’s pathology, may mediate the association between ApoE4 and slow gait among elderly individuals with pathological cognitive impairment.</description><issn>1552-5260</issn><issn>1552-5279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNo9UMtKw0AUDaJgrW78gvsDqTN5110oVQvFgnTlJtxMbpKRZKbMTAz6e_6YaSuu7jmX84DjefecLThjwQN23wsWRXHELrwZj-PAj4N0efmPE3bt3Vj7wVjEMh7PvJ-8VNr02EFpUCqwzgzCDYagp0qiIwuuJUBrtZio1ApKciORgvyg1xGgqsB2eoQGpQPstWrgMAlJOQujdO2RtbrTjRRTi9CNkk5-Esj-gNL0k-4R3sgO3aSvje5PfTvl0EgNrzQYXVFDigyebJOU0IgWNsec0-_Wu6qxs3T3d-fe_mm9X734293zZpVv_SHNmC-4yDKBSZAEIQYspToNqyUPyyyq6iqjUNRRlrAopLTMkKFgiFWwZGVdxUSTae7xc-woO_oqDkb2aL4Kzorj9MU0fXGevsi372cU_gKQdYBc</recordid><startdate>202012</startdate><enddate>202012</enddate><creator>Sakurai, Ryota</creator><creator>Faria‐Pieruccini, Frederico</creator><creator>Dilliott, Allison Ann</creator><creator>Hegele, Robert</creator><creator>Tartaglia, Carmela</creator><creator>McLaughlin, Paula</creator><creator>Binns, Malcolm</creator><creator>Blue, Korbin</creator><creator>Cornish, Ben</creator><creator>Sunderland, Kelly M</creator><creator>Beaton, Derek</creator><creator>Haddad, Seyyed M.H.</creator><creator>Tan, Brian</creator><creator>Swartz, Richard H.</creator><creator>Kwan, Donna</creator><creator>Masellis, Mario</creator><creator>Ramirez, Joel</creator><creator>Roberts, Angela C</creator><creator>Black, Sandra E.</creator><creator>Symons, Sean</creator><creator>Strother, Stephen C</creator><creator>Borrie, Michael</creator><creator>Pasternak, Stephen H.</creator><creator>Freedman, Morris</creator><creator>Bartha, Robert</creator><creator>Lang, Anthony</creator><creator>Munoz, Douglas</creator><creator>McIlroy, Bill</creator><creator>Montero‐Odasso, Manuel</creator><scope/></search><sort><creationdate>202012</creationdate><title>Abnormal brain structure mediates the association between ApoE4 and slow gait among patients with pathological cognitive impairment: Results from the Ontario Neurodegenerative Research Initiative</title><author>Sakurai, Ryota ; Faria‐Pieruccini, Frederico ; Dilliott, Allison Ann ; Hegele, Robert ; Tartaglia, Carmela ; McLaughlin, Paula ; Binns, Malcolm ; Blue, Korbin ; Cornish, Ben ; Sunderland, Kelly M ; Beaton, Derek ; Haddad, Seyyed M.H. ; Tan, Brian ; Swartz, Richard H. ; Kwan, Donna ; Masellis, Mario ; Ramirez, Joel ; Roberts, Angela C ; Black, Sandra E. ; Symons, Sean ; Strother, Stephen C ; Borrie, Michael ; Pasternak, Stephen H. ; Freedman, Morris ; Bartha, Robert ; Lang, Anthony ; Munoz, Douglas ; McIlroy, Bill ; Montero‐Odasso, Manuel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-u780-c1c88ca62623a207ef73d913b84dfd8e3cf486043e7b8a0ac0aad290bfd5ee623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sakurai, Ryota</creatorcontrib><creatorcontrib>Faria‐Pieruccini, Frederico</creatorcontrib><creatorcontrib>Dilliott, Allison Ann</creatorcontrib><creatorcontrib>Hegele, Robert</creatorcontrib><creatorcontrib>Tartaglia, Carmela</creatorcontrib><creatorcontrib>McLaughlin, Paula</creatorcontrib><creatorcontrib>Binns, Malcolm</creatorcontrib><creatorcontrib>Blue, Korbin</creatorcontrib><creatorcontrib>Cornish, Ben</creatorcontrib><creatorcontrib>Sunderland, Kelly M</creatorcontrib><creatorcontrib>Beaton, Derek</creatorcontrib><creatorcontrib>Haddad, Seyyed M.H.</creatorcontrib><creatorcontrib>Tan, Brian</creatorcontrib><creatorcontrib>Swartz, Richard H.</creatorcontrib><creatorcontrib>Kwan, Donna</creatorcontrib><creatorcontrib>Masellis, Mario</creatorcontrib><creatorcontrib>Ramirez, Joel</creatorcontrib><creatorcontrib>Roberts, Angela C</creatorcontrib><creatorcontrib>Black, Sandra E.</creatorcontrib><creatorcontrib>Symons, Sean</creatorcontrib><creatorcontrib>Strother, Stephen C</creatorcontrib><creatorcontrib>Borrie, Michael</creatorcontrib><creatorcontrib>Pasternak, Stephen H.</creatorcontrib><creatorcontrib>Freedman, Morris</creatorcontrib><creatorcontrib>Bartha, Robert</creatorcontrib><creatorcontrib>Lang, Anthony</creatorcontrib><creatorcontrib>Munoz, Douglas</creatorcontrib><creatorcontrib>McIlroy, Bill</creatorcontrib><creatorcontrib>Montero‐Odasso, Manuel</creatorcontrib><jtitle>Alzheimer's & dementia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sakurai, Ryota</au><au>Faria‐Pieruccini, Frederico</au><au>Dilliott, Allison Ann</au><au>Hegele, Robert</au><au>Tartaglia, Carmela</au><au>McLaughlin, Paula</au><au>Binns, Malcolm</au><au>Blue, Korbin</au><au>Cornish, Ben</au><au>Sunderland, Kelly M</au><au>Beaton, Derek</au><au>Haddad, Seyyed M.H.</au><au>Tan, Brian</au><au>Swartz, Richard H.</au><au>Kwan, Donna</au><au>Masellis, Mario</au><au>Ramirez, Joel</au><au>Roberts, Angela C</au><au>Black, Sandra E.</au><au>Symons, Sean</au><au>Strother, Stephen C</au><au>Borrie, Michael</au><au>Pasternak, Stephen H.</au><au>Freedman, Morris</au><au>Bartha, Robert</au><au>Lang, Anthony</au><au>Munoz, Douglas</au><au>McIlroy, Bill</au><au>Montero‐Odasso, Manuel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abnormal brain structure mediates the association between ApoE4 and slow gait among patients with pathological cognitive impairment: Results from the Ontario Neurodegenerative Research Initiative</atitle><jtitle>Alzheimer's & dementia</jtitle><date>2020-12</date><risdate>2020</risdate><volume>16</volume><epage>n/a</epage><issn>1552-5260</issn><eissn>1552-5279</eissn><abstract>Background
Presence of at least one copy of the polymorphic apolipoprotein E ε4 allele (ApoE4) increases the risk of impairments of gait performance, particularly in elderly individuals with cognitive impairment or at risk of dementia; however, its underlying neural mechanism are unclear. This study examined the association among ApoE4, gait performance, and brain structural changes among elderly individuals with cognitive impairment.
Method
Overall, 269 older adults with Alzheimer’s disease, cerebrovascular disease with and without cognitive impairment, and mild cognitive impairment were included from the Ontario Neurodegenerative Disease Research Initiative, who were either ApoE4 carriers (n=98) or non‐ApoE4 (n=171) carriers. Gait speed was measured using an electronic walkway; speed <1 m/s was defined as slow gait. Participants were stratified into four groups according to the presence of at least one copy of ApoE4 and slow gait. Region of interest volumes were derived by automated segmentation using a 3.0T magnetic resonance imaging system.
Result
Among ApoE4 carriers, 65 (24.2%) participants had slow gait. ApoE4 carriers with slow gait showed significantly higher burden of white matter hyperintensities compared with ApoE4 carriers without slow gait. Moreover, they had significantly lower hippocampal volume and greater total sulcal cerebrospinal fluid volume compared with non‐ApoE4 carriers with slow gait. These differences remained significant despite controlling for covariates (e.g., demographic and clinical characteristics, including participant type).
Conclusion
Our results suggest that brain structural changes, attributable to Alzheimer’s pathology, may mediate the association between ApoE4 and slow gait among elderly individuals with pathological cognitive impairment.</abstract><doi>10.1002/alz.044540</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| title | Abnormal brain structure mediates the association between ApoE4 and slow gait among patients with pathological cognitive impairment: Results from the Ontario Neurodegenerative Research Initiative |
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