Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 55-62 |
| Number of pages | 8 |
| Journal | Neurobiol. Aging |
| Volume | 89 |
| DOIs | |
| Publication status | Published - 2020 |
Keywords
- Alzheimer's disease
- Apolipoprotein E
- CSF cutoff
- Disease progression
- Mild cognitive impairment
- amyloid beta protein[1-42]
- apolipoprotein E
- apolipoprotein E epsilon4
- tau protein
- unclassified drug
- amyloid beta protein
- amyloid beta-protein (1-42)
- biological marker
- peptide fragment
- age distribution
- aged
- Alzheimer disease
- Article
- brain atrophy
- cerebrospinal fluid
- cohort analysis
- controlled study
- diagnostic accuracy
- diagnostic test accuracy study
- early diagnosis
- female
- genotype
- heterozygote
- hippocampus
- human
- major clinical study
- male
- mild cognitive impairment
- neuroimaging
- priority journal
- protein cerebrospinal fluid level
- receiver operating characteristic
- sensitivity and specificity
- sex difference
- validity
- white matter lesion
- cognitive defect
- complication
- genetics
- very elderly
- Aged
- Aged, 80 and over
- Alzheimer Disease
- Amyloid beta-Peptides
- Apolipoproteins E
- Biomarkers
- Cognitive Dysfunction
- Cohort Studies
- Female
- Heterozygote
- Humans
- Male
- Peptide Fragments
- tau Proteins
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CSF cutoffs for MCI due to AD depend on APOEε4 carrier status : Neurobiology of Aging. / Marizzoni, M.; Ferrari, C.; Babiloni, C.; Albani, D.; Barkhof, F.; Cavaliere, L.; Didic, M.; Forloni, G.; Fusco, F.; Galluzzi, S.; Hensch, T.; Jovicich, J.; Marra, C.; Molinuevo, J.L.; Nobili, F.; Parnetti, L.; Payoux, P.; Ranjeva, J.-P.; Ribaldi, F.; Rolandi, E.; Rossini, P.M.; Salvatore, M.; Soricelli, A.; Tsolaki, M.; Visser, P.J.; Wiltfang, J.; Richardson, J.C.; Bordet, R.; Blin, O.; Frisoni, G.B.
In: Neurobiol. Aging, Vol. 89, 2020, p. 55-62.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - CSF cutoffs for MCI due to AD depend on APOEε4 carrier status
T2 - Neurobiology of Aging
AU - Marizzoni, M.
AU - Ferrari, C.
AU - Babiloni, C.
AU - Albani, D.
AU - Barkhof, F.
AU - Cavaliere, L.
AU - Didic, M.
AU - Forloni, G.
AU - Fusco, F.
AU - Galluzzi, S.
AU - Hensch, T.
AU - Jovicich, J.
AU - Marra, C.
AU - Molinuevo, J.L.
AU - Nobili, F.
AU - Parnetti, L.
AU - Payoux, P.
AU - Ranjeva, J.-P.
AU - Ribaldi, F.
AU - Rolandi, E.
AU - Rossini, P.M.
AU - Salvatore, M.
AU - Soricelli, A.
AU - Tsolaki, M.
AU - Visser, P.J.
AU - Wiltfang, J.
AU - Richardson, J.C.
AU - Bordet, R.
AU - Blin, O.
AU - Frisoni, G.B.
N1 - Cited By :2 Export Date: 16 February 2021 CODEN: NEAGD Correspondence Address: Marizzoni, M.; Laboratory of Neuroimaging and Alzheimer's Epidemiology, via Pilastroni 4, Italy; email: mmarizzoni@fatebenefratelli.eu Chemicals/CAS: amyloid beta protein, 109770-29-8; Amyloid beta-Peptides; amyloid beta-protein (1-42); Apolipoproteins E; Biomarkers; Peptide Fragments; tau Proteins Funding details: 115009 Funding details: National Institute for Health Research, NIHR Funding details: Alzheimer's Association, AA, GEENA-Q-19-595850 Funding details: University College London Hospitals NHS Foundation Trust, UCLH Funding details: Seventh Framework Programme, FP7 Funding text 1: The research leading to the present results has received funding from the European Community's Seventh Framework Programme (FP7/2007-2013) for the Innovative Medicine Initiative under grant agreement n°115009 (Prediction of cognitive properties of new drug candidates for neurodegenerative diseases in early clinical development, PharmaCog) and from the Alzheimer's Association under grant agreement n° GEENA-Q-19-595850 (The dark side of APOE ε4: unraveling amyloid-independent effects in AD). FB is supported by the NIHR biomedical research centre at UCLH. References: Albert, M.S., Steven, D., Dickson, D., Dubois, B., Feldman, H.H., Fox, N.C., Gamst, A., Phelps, C.H., The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease (2011) Alzheimers Dement., 7, pp. 270-279; Altmann, A., Tian, L., Henderson, V.W., Greicius, M.D., Sex modifies the APOE-related risk of developing Alzheimer disease (2014) Ann. Neurol., 75, pp. 563-573; Andrews-Zwilling, Y., Bien-Ly, N., Xu, Q., Li, G., Bernardo, A., Yoon, S.Y., Zwilling, D., Huang, Y., Apolipoprotein E4 causes age- and tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice (2010) J. 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PY - 2020
Y1 - 2020
N2 - Amyloid and tau pathological accumulation should be considered for Alzheimer's disease (AD) definition and before subjects' enrollment in disease-modifying trials. Although age, APOEε4, and sex influence cerebrospinal fluid (CSF) biomarker levels, none of these variables are considered by current normality/abnormality cutoffs. Using baseline CSF data from 2 independent cohorts (PharmaCOG/European Alzheimer's Disease Neuroimaging Initiative and Alzheimer's Disease Neuroimaging Initiative), we investigated the effect of age, APOEε4 status, and sex on CSF Aβ42/P-tau distribution and cutoff extraction by applying mixture models with covariates. The Aβ42/P-tau distribution revealed the presence of 3 subgroups (AD-like, intermediate, control-like) and 2 cutoffs. The identification of the intermediate subgroup and of the higher cutoff was APOEε4 dependent in both cohorts. APOE-specific classification (higher cutoff for APOEε4+, lower cutoff for APOEε4-) showed higher diagnostic accuracy in identifying MCI due to AD compared to single Aβ42 and Aβ42/P-tau cutoffs. APOEε4 influences amyloid and tau CSF markers and AD progression in MCI patients supporting i) the use of APOE-specific cutoffs to identify MCI due to AD and ii) the utility of considering APOE genotype for early AD diagnosis. © 2020 Elsevier Inc.
AB - Amyloid and tau pathological accumulation should be considered for Alzheimer's disease (AD) definition and before subjects' enrollment in disease-modifying trials. Although age, APOEε4, and sex influence cerebrospinal fluid (CSF) biomarker levels, none of these variables are considered by current normality/abnormality cutoffs. Using baseline CSF data from 2 independent cohorts (PharmaCOG/European Alzheimer's Disease Neuroimaging Initiative and Alzheimer's Disease Neuroimaging Initiative), we investigated the effect of age, APOEε4 status, and sex on CSF Aβ42/P-tau distribution and cutoff extraction by applying mixture models with covariates. The Aβ42/P-tau distribution revealed the presence of 3 subgroups (AD-like, intermediate, control-like) and 2 cutoffs. The identification of the intermediate subgroup and of the higher cutoff was APOEε4 dependent in both cohorts. APOE-specific classification (higher cutoff for APOEε4+, lower cutoff for APOEε4-) showed higher diagnostic accuracy in identifying MCI due to AD compared to single Aβ42 and Aβ42/P-tau cutoffs. APOEε4 influences amyloid and tau CSF markers and AD progression in MCI patients supporting i) the use of APOE-specific cutoffs to identify MCI due to AD and ii) the utility of considering APOE genotype for early AD diagnosis. © 2020 Elsevier Inc.
KW - Alzheimer's disease
KW - Apolipoprotein E
KW - CSF cutoff
KW - Disease progression
KW - Mild cognitive impairment
KW - amyloid beta protein[1-42]
KW - apolipoprotein E
KW - apolipoprotein E epsilon4
KW - tau protein
KW - unclassified drug
KW - amyloid beta protein
KW - amyloid beta-protein (1-42)
KW - biological marker
KW - peptide fragment
KW - age distribution
KW - aged
KW - Alzheimer disease
KW - Article
KW - brain atrophy
KW - cerebrospinal fluid
KW - cohort analysis
KW - controlled study
KW - diagnostic accuracy
KW - diagnostic test accuracy study
KW - early diagnosis
KW - female
KW - genotype
KW - heterozygote
KW - hippocampus
KW - human
KW - major clinical study
KW - male
KW - mild cognitive impairment
KW - neuroimaging
KW - priority journal
KW - protein cerebrospinal fluid level
KW - receiver operating characteristic
KW - sensitivity and specificity
KW - sex difference
KW - validity
KW - white matter lesion
KW - cognitive defect
KW - complication
KW - genetics
KW - very elderly
KW - Aged
KW - Aged, 80 and over
KW - Alzheimer Disease
KW - Amyloid beta-Peptides
KW - Apolipoproteins E
KW - Biomarkers
KW - Cognitive Dysfunction
KW - Cohort Studies
KW - Female
KW - Heterozygote
KW - Humans
KW - Male
KW - Peptide Fragments
KW - tau Proteins
U2 - 10.1016/j.neurobiolaging.2019.12.019
DO - 10.1016/j.neurobiolaging.2019.12.019
M3 - Article
VL - 89
SP - 55
EP - 62
JO - Neurobiol. Aging
JF - Neurobiol. Aging
SN - 0197-4580
ER -