Amyloid-β associated volume loss occurs only in the presence of phospho-tau
The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid‐β (Aβ) and tau, is still unclear. Here, we examined 286 nondemented participants (107 cognitively normal older adults and 179 memory impaired individuals) who underwent longitudinal magnetic r...
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| Published in | Annals of neurology Vol. 70; no. 4; pp. 657 - 661 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.10.2011
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| Abstract | The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid‐β (Aβ) and tau, is still unclear. Here, we examined 286 nondemented participants (107 cognitively normal older adults and 179 memory impaired individuals) who underwent longitudinal magnetic resonance (MR) imaging and lumbar puncture. Using mixed effects models, we investigated the relationship between longitudinal entorhinal cortex atrophy rate, cerebrospinal fluid (CSF) p‐tau181p and CSF Aβ1–42. We found a significant relationship between elevated entorhinal cortex atrophy rate and decreased CSF Aβ1–42 only with elevated CSF p‐tau181p. Our findings indicate that Aβ‐associated volume loss occurs only in the presence of phospho‐tau in humans at risk for dementia. Ann Neurol 2011 |
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| AbstractList | The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid‐β (Aβ) and tau, is still unclear. Here, we examined 286 nondemented participants (107 cognitively normal older adults and 179 memory impaired individuals) who underwent longitudinal magnetic resonance (MR) imaging and lumbar puncture. Using mixed effects models, we investigated the relationship between longitudinal entorhinal cortex atrophy rate, cerebrospinal fluid (CSF) p‐tau181p and CSF Aβ1–42. We found a significant relationship between elevated entorhinal cortex atrophy rate and decreased CSF Aβ1–42 only with elevated CSF p‐tau181p. Our findings indicate that Aβ‐associated volume loss occurs only in the presence of phospho‐tau in humans at risk for dementia. Ann Neurol 2011 Abstract The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid‐β (Aβ) and tau, is still unclear. Here, we examined 286 nondemented participants (107 cognitively normal older adults and 179 memory impaired individuals) who underwent longitudinal magnetic resonance (MR) imaging and lumbar puncture. Using mixed effects models, we investigated the relationship between longitudinal entorhinal cortex atrophy rate, cerebrospinal fluid (CSF) p‐tau 181p and CSF Aβ 1–42 . We found a significant relationship between elevated entorhinal cortex atrophy rate and decreased CSF Aβ 1–42 only with elevated CSF p‐tau 181p . Our findings indicate that Aβ‐associated volume loss occurs only in the presence of phospho‐tau in humans at risk for dementia. Ann Neurol 2011 The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid-β (Aβ) and tau, is still unclear. Here, we examined 286 nondemented participants (107 cognitively normal older adults and 179 memory impaired individuals) who underwent longitudinal magnetic resonance (MR) imaging and lumbar puncture. Using mixed effects models, we investigated the relationship between longitudinal entorhinal cortex atrophy rate, cerebrospinal fluid (CSF) p-tau(181p) and CSF Aβ(1-42) . We found a significant relationship between elevated entorhinal cortex atrophy rate and decreased CSF Aβ(1-42) only with elevated CSF p-tau(181p) . Our findings indicate that Aβ-associated volume loss occurs only in the presence of phospho-tau in humans at risk for dementia. The relationship between neurodegeneration and the two hallmark proteins of Alzheimer's disease, amyloid-β (Aβ) and tau, is still unclear. Here, we examined 286 non-demented participants (107 cognitively normal older adults and 179 memory impaired individuals) who underwent longitudinal MR imaging and lumbar puncture. Using mixed effects models, we investigated the relationship between longitudinal entorhinal cortex atrophy, CSF p-tau 181p and CSF Aβ 1-42 . We found a significant relationship between elevated entorhinal cortex atrophy and decreased CSF Aβ 1-42 only with elevated CSF p-tau 181p . Our findings indicate that Aβ-associated volume loss occurs only in the presence of phospho-tauin humans at risk for dementia. |
| Author | Desikan, Rahul S. Brewer, James B. Roddey, J. Cooper McEvoy, Linda K. Thompson, Wesley K. Blennow, Kaj Dale, Anders M. Holland, Dominic Aisen, Paul S. Hyman, Bradley T. |
| AuthorAffiliation | 5 Department of Neurology, Massachusetts General Hospital, Boston, MA, USA 3 Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA 1 Department of Radiology, University of California, San Diego, La Jolla, CA, USA 2 Department of Neuroscience, University of California, San Diego, La Jolla, CA, USA 4 Clinical Neurochemistry Laboratory, The Sahlgrenska Academy at Göteburg University, Mölndal, 40530, Gotheburg, Sweden |
| AuthorAffiliation_xml | – name: 2 Department of Neuroscience, University of California, San Diego, La Jolla, CA, USA – name: 3 Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA – name: 4 Clinical Neurochemistry Laboratory, The Sahlgrenska Academy at Göteburg University, Mölndal, 40530, Gotheburg, Sweden – name: 1 Department of Radiology, University of California, San Diego, La Jolla, CA, USA – name: 5 Department of Neurology, Massachusetts General Hospital, Boston, MA, USA |
| Author_xml | – sequence: 1 givenname: Rahul S. surname: Desikan fullname: Desikan, Rahul S. organization: Department Radiology, University of California, San Diego, La Jolla, CA – sequence: 2 givenname: Linda K. surname: McEvoy fullname: McEvoy, Linda K. organization: Department Radiology, University of California, San Diego, La Jolla, CA – sequence: 3 givenname: Wesley K. surname: Thompson fullname: Thompson, Wesley K. organization: Department Psychiatry, University of California, San Diego, La Jolla, CA – sequence: 4 givenname: Dominic surname: Holland fullname: Holland, Dominic organization: Department Neuroscience, University of California, San Diego, La Jolla, CA – sequence: 5 givenname: J. Cooper surname: Roddey fullname: Roddey, J. Cooper organization: Department Neuroscience, University of California, San Diego, La Jolla, CA – sequence: 6 givenname: Kaj surname: Blennow fullname: Blennow, Kaj organization: Clinical Neurochemistry Laboratory, The Sahlgrenska Academy at Göteburg University, Götheburg, Sweden – sequence: 7 givenname: Paul S. surname: Aisen fullname: Aisen, Paul S. organization: Department Neuroscience, University of California, San Diego, La Jolla, CA – sequence: 8 givenname: James B. surname: Brewer fullname: Brewer, James B. organization: Department Radiology, University of California, San Diego, La Jolla, CA – sequence: 9 givenname: Bradley T. surname: Hyman fullname: Hyman, Bradley T. organization: Department of Neurology, Massachusetts General Hospital, Boston, MA – sequence: 10 givenname: Anders M. surname: Dale fullname: Dale, Anders M. email: amdale@ucsd.edu organization: Department Radiology, University of California, San Diego, La Jolla, CA |
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| Keywords | Nervous system diseases Amyloid |
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| Notes | istex:5A61294777A93211BE2CBE186500FFCA7A687D7D ArticleID:ANA22509 ark:/67375/WNG-GWFRL8LX-5 Information about the Alzheimer's Disease Neuroimaging Initiative is listed in the Appendix on page xx. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Data used in the preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (www.loni.ucla.edu/ADNI). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. ADNI investigators include (complete listing available at http://adni.loni.ucla.edu/wp-content/uploads/how_to_apply/ADNI_Authorship_List.pdf |
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| Snippet | The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid‐β (Aβ) and tau, is still unclear. Here, we examined 286... The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid-β (Aβ) and tau, is still unclear. Here, we examined 286... Abstract The relationship between neurodegeneration and the 2 hallmark proteins of Alzheimer's disease, amyloid‐β (Aβ) and tau, is still unclear. Here, we... The relationship between neurodegeneration and the two hallmark proteins of Alzheimer's disease, amyloid-β (Aβ) and tau, is still unclear. Here, we examined... |
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| SubjectTerms | 80 and over Aged Aged, 80 and over Amnesia Amnesia - cerebrospinal fluid Amnesia - pathology Amyloid beta-Peptides Amyloid beta-Peptides - cerebrospinal fluid Atrophy Biological and medical sciences Cerebral Cortex Cerebral Cortex - pathology cerebrospinal fluid Cognitive Dysfunction - cerebrospinal fluid Cognitive Dysfunction - pathology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Humans Longitudinal Studies Male Medical sciences Mild Cognitive Impairment Neurology pathology Peptide Fragments Peptide Fragments - cerebrospinal fluid Psychiatry Psykiatri tau Proteins tau Proteins - cerebrospinal fluid |
| Title | Amyloid-β associated volume loss occurs only in the presence of phospho-tau |
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