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Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network

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Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network. / Benson, Gloria S; Bauer, Chris; Hausner, Lucrezia; Couturier, Samuel; Lewczuk, Piotr; Peters, Oliver; Hüll, Michael; Jahn, Holger; Jessen, Frank; Pantel, Johannes; Teipel, Stefan J; Wagner, Michael; Schuchhardt, Johannes; Wiltfang, Jens; Kornhuber, Johannes; Frölich, Lutz.

In: J NEURAL TRANSM, Vol. 129, No. 5-6, 06.2022, p. 477-486.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Benson, GS, Bauer, C, Hausner, L, Couturier, S, Lewczuk, P, Peters, O, Hüll, M, Jahn, H, Jessen, F, Pantel, J, Teipel, SJ, Wagner, M, Schuchhardt, J, Wiltfang, J, Kornhuber, J & Frölich, L 2022, 'Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network', J NEURAL TRANSM, vol. 129, no. 5-6, pp. 477-486. https://doi.org/10.1007/s00702-022-02461-0

APA

Benson, G. S., Bauer, C., Hausner, L., Couturier, S., Lewczuk, P., Peters, O., Hüll, M., Jahn, H., Jessen, F., Pantel, J., Teipel, S. J., Wagner, M., Schuchhardt, J., Wiltfang, J., Kornhuber, J., & Frölich, L. (2022). Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network. J NEURAL TRANSM, 129(5-6), 477-486. https://doi.org/10.1007/s00702-022-02461-0

Vancouver

Benson GS, Bauer C, Hausner L, Couturier S, Lewczuk P, Peters O et al. Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network. J NEURAL TRANSM. 2022 Jun;129(5-6):477-486. https://doi.org/10.1007/s00702-022-02461-0

Bibtex

@article{e4ac2584554448aea3b12f3d1a9ebc8b,
title = "Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network",
abstract = "ApoE4, the strongest genetic risk factor for Alzheimer's disease (AD), has been shown to be associated with both beta-amyloid (Aβ) and tau pathology, with the strongest evidence for effects on Aβ, while the association between ApoE4 and tau pathology remains inconsistent. This study aimed to investigate the associations between ApoE4 with CSF Aβ42, total tau (t-tau), phospho-tau181 (p-tau), and with the progression of decline in a large cohort of MCI subjects, both progressors to AD and other dementias, as well as non-progressors. We analyzed associations of CSF Aβ42, p-tau and t-tau with ApoE4 allele frequency cross-sectionally and longitudinally over 3 years of follow-up in 195 individuals with a diagnosis of MCI-stable, MCI-AD converters and MCI progressing to other dementias from the German Dementia Competence Network. In the total sample, ApoE4 carriers had lower concentrations of CSF Aβ42, and increased concentrations of t-tau and p-tau compared to non-carriers in a gene dose-dependent manner. Comparisons of these associations stratified by MCI-progression groups showed a significant influence of ApoE4 carriership and diagnostic group on all CSF biomarker levels. The effect of ApoE4 was present in MCI-stable individuals but not in the other groups, with ApoE4 + carriers having decreased CSF Aβ 42 levels, and increased concentration of t-tau and p-tau. Longitudinally, individuals with abnormal t-tau and Aβ42 had a more rapid progression of cognitive and clinical decline, independently of ApoE4 genotype. Overall, our results contribute to an emerging framework in which ApoE4 involves mechanisms associated with both CSF amyloid-β burden and tau aggregation at specific time points in AD pathogenesis.",
author = "Benson, {Gloria S} and Chris Bauer and Lucrezia Hausner and Samuel Couturier and Piotr Lewczuk and Oliver Peters and Michael H{\"u}ll and Holger Jahn and Frank Jessen and Johannes Pantel and Teipel, {Stefan J} and Michael Wagner and Johannes Schuchhardt and Jens Wiltfang and Johannes Kornhuber and Lutz Fr{\"o}lich",
note = "{\textcopyright} 2022. The Author(s).",
year = "2022",
month = jun,
doi = "10.1007/s00702-022-02461-0",
language = "English",
volume = "129",
pages = "477--486",
journal = "J NEURAL TRANSM",
issn = "0300-9564",
publisher = "Springer",
number = "5-6",

}

RIS

TY - JOUR

T1 - Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network

AU - Benson, Gloria S

AU - Bauer, Chris

AU - Hausner, Lucrezia

AU - Couturier, Samuel

AU - Lewczuk, Piotr

AU - Peters, Oliver

AU - Hüll, Michael

AU - Jahn, Holger

AU - Jessen, Frank

AU - Pantel, Johannes

AU - Teipel, Stefan J

AU - Wagner, Michael

AU - Schuchhardt, Johannes

AU - Wiltfang, Jens

AU - Kornhuber, Johannes

AU - Frölich, Lutz

N1 - © 2022. The Author(s).

PY - 2022/6

Y1 - 2022/6

N2 - ApoE4, the strongest genetic risk factor for Alzheimer's disease (AD), has been shown to be associated with both beta-amyloid (Aβ) and tau pathology, with the strongest evidence for effects on Aβ, while the association between ApoE4 and tau pathology remains inconsistent. This study aimed to investigate the associations between ApoE4 with CSF Aβ42, total tau (t-tau), phospho-tau181 (p-tau), and with the progression of decline in a large cohort of MCI subjects, both progressors to AD and other dementias, as well as non-progressors. We analyzed associations of CSF Aβ42, p-tau and t-tau with ApoE4 allele frequency cross-sectionally and longitudinally over 3 years of follow-up in 195 individuals with a diagnosis of MCI-stable, MCI-AD converters and MCI progressing to other dementias from the German Dementia Competence Network. In the total sample, ApoE4 carriers had lower concentrations of CSF Aβ42, and increased concentrations of t-tau and p-tau compared to non-carriers in a gene dose-dependent manner. Comparisons of these associations stratified by MCI-progression groups showed a significant influence of ApoE4 carriership and diagnostic group on all CSF biomarker levels. The effect of ApoE4 was present in MCI-stable individuals but not in the other groups, with ApoE4 + carriers having decreased CSF Aβ 42 levels, and increased concentration of t-tau and p-tau. Longitudinally, individuals with abnormal t-tau and Aβ42 had a more rapid progression of cognitive and clinical decline, independently of ApoE4 genotype. Overall, our results contribute to an emerging framework in which ApoE4 involves mechanisms associated with both CSF amyloid-β burden and tau aggregation at specific time points in AD pathogenesis.

AB - ApoE4, the strongest genetic risk factor for Alzheimer's disease (AD), has been shown to be associated with both beta-amyloid (Aβ) and tau pathology, with the strongest evidence for effects on Aβ, while the association between ApoE4 and tau pathology remains inconsistent. This study aimed to investigate the associations between ApoE4 with CSF Aβ42, total tau (t-tau), phospho-tau181 (p-tau), and with the progression of decline in a large cohort of MCI subjects, both progressors to AD and other dementias, as well as non-progressors. We analyzed associations of CSF Aβ42, p-tau and t-tau with ApoE4 allele frequency cross-sectionally and longitudinally over 3 years of follow-up in 195 individuals with a diagnosis of MCI-stable, MCI-AD converters and MCI progressing to other dementias from the German Dementia Competence Network. In the total sample, ApoE4 carriers had lower concentrations of CSF Aβ42, and increased concentrations of t-tau and p-tau compared to non-carriers in a gene dose-dependent manner. Comparisons of these associations stratified by MCI-progression groups showed a significant influence of ApoE4 carriership and diagnostic group on all CSF biomarker levels. The effect of ApoE4 was present in MCI-stable individuals but not in the other groups, with ApoE4 + carriers having decreased CSF Aβ 42 levels, and increased concentration of t-tau and p-tau. Longitudinally, individuals with abnormal t-tau and Aβ42 had a more rapid progression of cognitive and clinical decline, independently of ApoE4 genotype. Overall, our results contribute to an emerging framework in which ApoE4 involves mechanisms associated with both CSF amyloid-β burden and tau aggregation at specific time points in AD pathogenesis.

U2 - 10.1007/s00702-022-02461-0

DO - 10.1007/s00702-022-02461-0

M3 - SCORING: Journal article

C2 - 35061102

VL - 129

SP - 477

EP - 486

JO - J NEURAL TRANSM

JF - J NEURAL TRANSM

SN - 0300-9564

IS - 5-6

ER -