Age, sex and APOE-ε4 modify the balance between soluble and fibrillar β-amyloid in non-demented individuals: topographical patterns across two independent cohorts

Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer’s continuum , which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). Yet, these biomarkers identify two distinct Aβ pools, reflecting the clearance of solubl...

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Published inMolecular psychiatry Vol. 27; no. 4; pp. 2010 - 2018
Main Authors Cacciaglia, Raffaele, Salvadó, Gemma, Molinuevo, José Luis, Shekari, Mahnaz, Falcon, Carles, Operto, Gregory, Suárez-Calvet, Marc, Milà-Alomà, Marta, Sala, Arianna, Rodriguez-Vieitez, Elena, Kollmorgen, Gwendlyn, Suridjan, Ivonne, Blennow, Kaj, Zetterberg, Henrik, Gispert, Juan Domingo
Format Journal Article Web Resource
LanguageEnglish
Published London Nature Publishing Group UK 01.04.2022
Nature Publishing Group
Springer Nature
Subjects
13/62
38/39
59/78
631/208
631/378
692/53
Age
Alzheimer Disease
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer's disease
Amyloid beta-Peptides
Amyloid beta-Peptides - metabolism
ApoE protein, human
Apolipoprotein E
Apolipoprotein E4
Apolipoprotein E4 - genetics
Apolipoproteins E
Apolipoproteins E - metabolism
Automotive Engineering
Behavioral Sciences
Biological Psychology
Biomarkers
Biomarkers - metabolism
Brain
Brain - metabolism
Cellular and Molecular Neuroscience
Cerebrospinal fluid
Female
Fibrils
Human health sciences
Humans
Localization
Male
Medicine
Medicine & Public Health
Molecular Biology
Neurologie
Neurology
Neurosciences
Pharmacotherapy
Positron emission tomography
Positron-Emission Tomography - methods
Psychiatry
Psychiatry and Mental Health
Risk factors
Sciences de la santé humaine
Sex
Tau protein
tau Proteins
tau Proteins - metabolism
Temporal lobe
β-Amyloid
Online AccessGet full text
ISSN1359-4184
1476-5578
1476-5578
DOI10.1038/s41380-022-01436-7

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Abstract Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer’s continuum , which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). Yet, these biomarkers identify two distinct Aβ pools, reflecting the clearance of soluble Aβ as opposed to the presence of Aβ fibrils in the brain. An open question is whether risk factors known to increase Alzheimer’s’ disease (AD) prevalence may promote an imbalance between soluble and deposited Aβ. Unveiling such interactions shall aid our understanding of the biological pathways underlying Aβ deposition and foster the design of effective prevention strategies. We assessed the impact of three major AD risk factors, such as age, APOE -ε4 and female sex, on the association between CSF and PET Aβ, in two independent samples of non-demented individuals (ALFA: n  = 320, ADNI: n  = 682). We tested our hypotheses both in candidate regions of interest and in the whole brain using voxel-wise non-parametric permutations. All of the assessed risk factors induced a higher Aβ deposition for any given level of CSF Aβ42/40, although in distinct cerebral topologies. While age and sex mapped onto neocortical areas, the effect of APOE -ε4 was prominent in the medial temporal lobe, which represents a target of early tau deposition. Further, we found that the effects of age and APOE -ε4 was stronger in women than in men. Our data indicate that specific AD risk factors affect the spatial patterns of cerebral Aβ aggregation, with APOE -ε4 possibly facilitating a co-localization between Aβ and tau along the disease continuum .
AbstractList Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer's continuum, which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). Yet, these biomarkers identify two distinct Aβ pools, reflecting the clearance of soluble Aβ as opposed to the presence of Aβ fibrils in the brain. An open question is whether risk factors known to increase Alzheimer's' disease (AD) prevalence may promote an imbalance between soluble and deposited Aβ. Unveiling such interactions shall aid our understanding of the biological pathways underlying Aβ deposition and foster the design of effective prevention strategies. We assessed the impact of three major AD risk factors, such as age, APOE-ε4 and female sex, on the association between CSF and PET Aβ, in two independent samples of non-demented individuals (ALFA: n = 320, ADNI: n = 682). We tested our hypotheses both in candidate regions of interest and in the whole brain using voxel-wise non-parametric permutations. All of the assessed risk factors induced a higher Aβ deposition for any given level of CSF Aβ42/40, although in distinct cerebral topologies. While age and sex mapped onto neocortical areas, the effect of APOE-ε4 was prominent in the medial temporal lobe, which represents a target of early tau deposition. Further, we found that the effects of age and APOE-ε4 was stronger in women than in men. Our data indicate that specific AD risk factors affect the spatial patterns of cerebral Aβ aggregation, with APOE-ε4 possibly facilitating a co-localization between Aβ and tau along the disease continuum.Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer's continuum, which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). Yet, these biomarkers identify two distinct Aβ pools, reflecting the clearance of soluble Aβ as opposed to the presence of Aβ fibrils in the brain. An open question is whether risk factors known to increase Alzheimer's' disease (AD) prevalence may promote an imbalance between soluble and deposited Aβ. Unveiling such interactions shall aid our understanding of the biological pathways underlying Aβ deposition and foster the design of effective prevention strategies. We assessed the impact of three major AD risk factors, such as age, APOE-ε4 and female sex, on the association between CSF and PET Aβ, in two independent samples of non-demented individuals (ALFA: n = 320, ADNI: n = 682). We tested our hypotheses both in candidate regions of interest and in the whole brain using voxel-wise non-parametric permutations. All of the assessed risk factors induced a higher Aβ deposition for any given level of CSF Aβ42/40, although in distinct cerebral topologies. While age and sex mapped onto neocortical areas, the effect of APOE-ε4 was prominent in the medial temporal lobe, which represents a target of early tau deposition. Further, we found that the effects of age and APOE-ε4 was stronger in women than in men. Our data indicate that specific AD risk factors affect the spatial patterns of cerebral Aβ aggregation, with APOE-ε4 possibly facilitating a co-localization between Aβ and tau along the disease continuum.
Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer’s continuum, which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). Yet, these biomarkers identify two distinct Aβ pools, reflecting the clearance of soluble Aβ as opposed to the presence of Aβ fibrils in the brain. An open question is whether risk factors known to increase Alzheimer’s’ disease (AD) prevalence may promote an imbalance between soluble and deposited Aβ. Unveiling such interactions shall aid our understanding of the biological pathways underlying Aβ deposition and foster the design of effective prevention strategies. We assessed the impact of three major AD risk factors, such as age, APOE-ε4 and female sex, on the association between CSF and PET Aβ, in two independent samples of non-demented individuals (ALFA: n = 320, ADNI: n = 682). We tested our hypotheses both in candidate regions of interest and in the whole brain using voxel-wise non-parametric permutations. All of the assessed risk factors induced a higher Aβ deposition for any given level of CSF Aβ42/40, although in distinct cerebral topologies. While age and sex mapped onto neocortical areas, the effect of APOE-ε4 was prominent in the medial temporal lobe, which represents a target of early tau deposition. Further, we found that the effects of age and APOE-ε4 was stronger in women than in men. Our data indicate that specific AD risk factors affect the spatial patterns of cerebral Aβ aggregation, with APOE-ε4 possibly facilitating a co-localization between Aβ and tau along the disease continuum.
Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer’s continuum , which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). Yet, these biomarkers identify two distinct Aβ pools, reflecting the clearance of soluble Aβ as opposed to the presence of Aβ fibrils in the brain. An open question is whether risk factors known to increase Alzheimer’s’ disease (AD) prevalence may promote an imbalance between soluble and deposited Aβ. Unveiling such interactions shall aid our understanding of the biological pathways underlying Aβ deposition and foster the design of effective prevention strategies. We assessed the impact of three major AD risk factors, such as age, APOE -ε4 and female sex, on the association between CSF and PET Aβ, in two independent samples of non-demented individuals (ALFA: n  = 320, ADNI: n  = 682). We tested our hypotheses both in candidate regions of interest and in the whole brain using voxel-wise non-parametric permutations. All of the assessed risk factors induced a higher Aβ deposition for any given level of CSF Aβ42/40, although in distinct cerebral topologies. While age and sex mapped onto neocortical areas, the effect of APOE -ε4 was prominent in the medial temporal lobe, which represents a target of early tau deposition. Further, we found that the effects of age and APOE -ε4 was stronger in women than in men. Our data indicate that specific AD risk factors affect the spatial patterns of cerebral Aβ aggregation, with APOE -ε4 possibly facilitating a co-localization between Aβ and tau along the disease continuum .
Author Shekari, Mahnaz
Falcon, Carles
Rodriguez-Vieitez, Elena
Operto, Gregory
Suridjan, Ivonne
Zetterberg, Henrik
Salvadó, Gemma
Gispert, Juan Domingo
Cacciaglia, Raffaele
Sala, Arianna
Molinuevo, José Luis
Blennow, Kaj
Milà-Alomà, Marta
Suárez-Calvet, Marc
Kollmorgen, Gwendlyn
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Snippet Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer’s continuum , which can be measured both in the cerebrospinal...
Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer's continuum, which can be measured both in the cerebrospinal...
Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer’s continuum, which can be measured both in the cerebrospinal...
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SubjectTerms 13/62
38/39
59/78
631/208
631/378
692/53
Age
Alzheimer Disease
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer's disease
Amyloid beta-Peptides
Amyloid beta-Peptides - metabolism
ApoE protein, human
Apolipoprotein E
Apolipoprotein E4
Apolipoprotein E4 - genetics
Apolipoproteins E
Apolipoproteins E - metabolism
Automotive Engineering
Behavioral Sciences
Biological Psychology
Biomarkers
Biomarkers - metabolism
Brain
Brain - metabolism
Cellular and Molecular Neuroscience
Cerebrospinal fluid
Female
Fibrils
Human health sciences
Humans
Localization
Male
Medicine
Medicine & Public Health
Molecular Biology
Neurologie
Neurology
Neurosciences
Pharmacotherapy
Positron emission tomography
Positron-Emission Tomography - methods
Psychiatry
Psychiatry and Mental Health
Risk factors
Sciences de la santé humaine
Sex
Tau protein
tau Proteins
tau Proteins - metabolism
Temporal lobe
β-Amyloid
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Title Age, sex and APOE-ε4 modify the balance between soluble and fibrillar β-amyloid in non-demented individuals: topographical patterns across two independent cohorts
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