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Prediction of Alzheimer disease in subjects with amnestic and nonamnestic MCI.

Vos, Stephanie J B; van Rossum, Ineke A; Verhey, Frans; Knol, Dirk L; Soininen, Hilkka; Wahlund, Lars-Olof; Hampel, Harald; Tsolaki, Magda; Minthon, Lennart LU and Frisoni, Giovanni B, et al. (2013) In Neurology 80(12). p.1124-1132
Abstract
OBJECTIVE: To compare the predictive accuracy of β-amyloid (Aβ)1-42 and total tau in CSF, hippocampal volume (HCV), and APOE genotype for Alzheimer disease (AD)-type dementia in subjects with amnestic mild cognitive impairment (aMCI) and nonamnestic mild cognitive impairment (naMCI). METHODS: We selected 399 subjects with aMCI and 226 subjects with naMCI from a multicenter memory clinic-based cohort. We measured CSF Aβ1-42 and tau by ELISA (n = 231), HCV on MRI (n = 388), and APOE ε4 (n = 523). Follow-up was performed annually up to 5 years. Outcome measures were progression to AD-type dementia and cognitive decline. RESULTS: At least 1 follow-up was available for 538 subjects (86%). One hundred thirty-two subjects with aMCI (38%) and 39... (More)
OBJECTIVE: To compare the predictive accuracy of β-amyloid (Aβ)1-42 and total tau in CSF, hippocampal volume (HCV), and APOE genotype for Alzheimer disease (AD)-type dementia in subjects with amnestic mild cognitive impairment (aMCI) and nonamnestic mild cognitive impairment (naMCI). METHODS: We selected 399 subjects with aMCI and 226 subjects with naMCI from a multicenter memory clinic-based cohort. We measured CSF Aβ1-42 and tau by ELISA (n = 231), HCV on MRI (n = 388), and APOE ε4 (n = 523). Follow-up was performed annually up to 5 years. Outcome measures were progression to AD-type dementia and cognitive decline. RESULTS: At least 1 follow-up was available for 538 subjects (86%). One hundred thirty-two subjects with aMCI (38%) and 39 subjects with naMCI (20%) progressed to AD-type dementia after an average follow-up of 2.5 years. CSF Aβ1-42, tau, Aβ1-42/tau ratio, HCV, and APOE ε4 predicted AD-type dementia in each MCI subgroup with the same overall diagnostic accuracy. However, CSF Aβ1-42 concentration was higher and hippocampal atrophy less severe in subjects with naMCI compared with aMCI. This reduced the sensitivity but increased the specificity of these markers for AD-type dementia in subjects with naMCI. CONCLUSIONS: AD biomarkers are useful to predict AD-type dementia in subjects with aMCI and naMCI. However, biomarkers might not be as sensitive for early diagnosis of AD in naMCI compared with aMCI. This may have implications for clinical implementation of the National Institute on Aging and Alzheimer's Association criteria. (Less)
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Contribution to journal
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published
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Neurology
volume
80
issue
12
pages
1124 - 1132
publisher
American Academy of Neurology
external identifiers
  • wos:000316674000014
  • pmid:23446677
  • scopus:84876256314
ISSN
1526-632X
DOI
10.1212/WNL.0b013e318288690c
language
English
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yes
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761f8483-c699-4221-bfcd-a8a3524fcab4 (old id 3628781)
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http://www.ncbi.nlm.nih.gov/pubmed/23446677?dopt=Abstract
date added to LUP
2013-04-03 08:48:18
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2019-07-07 03:24:10
@article{761f8483-c699-4221-bfcd-a8a3524fcab4,
  abstract     = {OBJECTIVE: To compare the predictive accuracy of β-amyloid (Aβ)1-42 and total tau in CSF, hippocampal volume (HCV), and APOE genotype for Alzheimer disease (AD)-type dementia in subjects with amnestic mild cognitive impairment (aMCI) and nonamnestic mild cognitive impairment (naMCI). METHODS: We selected 399 subjects with aMCI and 226 subjects with naMCI from a multicenter memory clinic-based cohort. We measured CSF Aβ1-42 and tau by ELISA (n = 231), HCV on MRI (n = 388), and APOE ε4 (n = 523). Follow-up was performed annually up to 5 years. Outcome measures were progression to AD-type dementia and cognitive decline. RESULTS: At least 1 follow-up was available for 538 subjects (86%). One hundred thirty-two subjects with aMCI (38%) and 39 subjects with naMCI (20%) progressed to AD-type dementia after an average follow-up of 2.5 years. CSF Aβ1-42, tau, Aβ1-42/tau ratio, HCV, and APOE ε4 predicted AD-type dementia in each MCI subgroup with the same overall diagnostic accuracy. However, CSF Aβ1-42 concentration was higher and hippocampal atrophy less severe in subjects with naMCI compared with aMCI. This reduced the sensitivity but increased the specificity of these markers for AD-type dementia in subjects with naMCI. CONCLUSIONS: AD biomarkers are useful to predict AD-type dementia in subjects with aMCI and naMCI. However, biomarkers might not be as sensitive for early diagnosis of AD in naMCI compared with aMCI. This may have implications for clinical implementation of the National Institute on Aging and Alzheimer's Association criteria.},
  author       = {Vos, Stephanie J B and van Rossum, Ineke A and Verhey, Frans and Knol, Dirk L and Soininen, Hilkka and Wahlund, Lars-Olof and Hampel, Harald and Tsolaki, Magda and Minthon, Lennart and Frisoni, Giovanni B and Froelich, Lutz and Nobili, Flavio and van der Flier, Wiesje and Blennow, Kaj and Wolz, Robin and Scheltens, Philip and Visser, Pieter Jelle},
  issn         = {1526-632X},
  language     = {eng},
  number       = {12},
  pages        = {1124--1132},
  publisher    = {American Academy of Neurology},
  series       = {Neurology},
  title        = {Prediction of Alzheimer disease in subjects with amnestic and nonamnestic MCI.},
  url          = {http://dx.doi.org/10.1212/WNL.0b013e318288690c},
  volume       = {80},
  year         = {2013},
}