Head-to-head comparison of plasma p-tau181, p-tau231 and glial fibrillary acidic protein in clinically unimpaired elderly with three levels of APOE4-related risk for Alzheimer's disease
Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional β-amyloid (Aβ) pathology and cognitive performance head-to-head in clinically...
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Published in | Neurobiology of disease Vol. 183; p. 106175 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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01.07.2023
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Abstract | Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional β-amyloid (Aβ) pathology and cognitive performance head-to-head in clinically unimpaired elderly (n = 88) at three levels of APOE4-related genetic risk for sporadic AD (APOE4/4 n = 19, APOE3/4 n = 32 or non-carriers n = 37). Concentrations of plasma p-tau181, p-tau231 and GFAP were measured using Single molecule array (Simoa), regional Aβ deposition with 11C-PiB positron emission tomography (PET), and cognitive performance with a preclinical composite. Significant differences in plasma p-tau181 and p-tau231, but not plasma GFAP concentrations were present between the APOE4 gene doses, explained solely by brain Aβ load. All plasma biomarkers correlated positively with Aβ PET in the total study population. This correlation was driven by APOE3/3 carriers for plasma p-tau markers and APOE4/4 carriers for plasma GFAP. Voxel-wise associations with amyloid-PET revealed different spatial patterns for plasma p-tau markers and plasma GFAP. Only higher plasma GFAP correlated with lower cognitive scores. Our observations suggest that plasma p-tau and plasma GFAP are both early AD markers reflecting different Aβ-related processes.
•Plasma p-tau181 and p-tau231 levels increase already in healthy APOE4 carriers.•Plasma p-tau markers and GFAP all associate with brain beta-amyloid load.•Only plasma GFAP associated with cross-sectional cognitive performance.•Plasma p-tau markers and plasma GFAP seem to reflect different Aβ related processes. |
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AbstractList | Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional β-amyloid (Aβ) pathology and cognitive performance head-to-head in clinically unimpaired elderly (n = 88) at three levels of APOE4-related genetic risk for sporadic AD (APOE4/4 n = 19, APOE3/4 n = 32 or non-carriers n = 37). Concentrations of plasma p-tau181, p-tau231 and GFAP were measured using Single molecule array (Simoa), regional Aβ deposition with 11C-PiB positron emission tomography (PET), and cognitive performance with a preclinical composite. Significant differences in plasma p-tau181 and p-tau231, but not plasma GFAP concentrations were present between the APOE4 gene doses, explained solely by brain Aβ load. All plasma biomarkers correlated positively with Aβ PET in the total study population. This correlation was driven by APOE3/3 carriers for plasma p-tau markers and APOE4/4 carriers for plasma GFAP. Voxel-wise associations with amyloid-PET revealed different spatial patterns for plasma p-tau markers and plasma GFAP. Only higher plasma GFAP correlated with lower cognitive scores. Our observations suggest that plasma p-tau and plasma GFAP are both early AD markers reflecting different Aβ-related processes.Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional β-amyloid (Aβ) pathology and cognitive performance head-to-head in clinically unimpaired elderly (n = 88) at three levels of APOE4-related genetic risk for sporadic AD (APOE4/4 n = 19, APOE3/4 n = 32 or non-carriers n = 37). Concentrations of plasma p-tau181, p-tau231 and GFAP were measured using Single molecule array (Simoa), regional Aβ deposition with 11C-PiB positron emission tomography (PET), and cognitive performance with a preclinical composite. Significant differences in plasma p-tau181 and p-tau231, but not plasma GFAP concentrations were present between the APOE4 gene doses, explained solely by brain Aβ load. All plasma biomarkers correlated positively with Aβ PET in the total study population. This correlation was driven by APOE3/3 carriers for plasma p-tau markers and APOE4/4 carriers for plasma GFAP. Voxel-wise associations with amyloid-PET revealed different spatial patterns for plasma p-tau markers and plasma GFAP. Only higher plasma GFAP correlated with lower cognitive scores. Our observations suggest that plasma p-tau and plasma GFAP are both early AD markers reflecting different Aβ-related processes. Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional β-amyloid (Aβ) pathology and cognitive performance head-to-head in clinically unimpaired elderly (n = 88) at three levels of APOE4-related genetic risk for sporadic AD (APOE4/4 n = 19, APOE3/4 n = 32 or non-carriers n = 37). Concentrations of plasma p-tau181, p-tau231 and GFAP were measured using Single molecule array (Simoa), regional Aβ deposition with 11C-PiB positron emission tomography (PET), and cognitive performance with a preclinical composite. Significant differences in plasma p-tau181 and p-tau231, but not plasma GFAP concentrations were present between the APOE4 gene doses, explained solely by brain Aβ load. All plasma biomarkers correlated positively with Aβ PET in the total study population. This correlation was driven by APOE3/3 carriers for plasma p-tau markers and APOE4/4 carriers for plasma GFAP. Voxel-wise associations with amyloid-PET revealed different spatial patterns for plasma p-tau markers and plasma GFAP. Only higher plasma GFAP correlated with lower cognitive scores. Our observations suggest that plasma p-tau and plasma GFAP are both early AD markers reflecting different Aβ-related processes. •Plasma p-tau181 and p-tau231 levels increase already in healthy APOE4 carriers.•Plasma p-tau markers and GFAP all associate with brain beta-amyloid load.•Only plasma GFAP associated with cross-sectional cognitive performance.•Plasma p-tau markers and plasma GFAP seem to reflect different Aβ related processes. Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional S-amyloid (AS) pathology and cognitive performance head-to-head in clinically unimpaired elderly (n = 88) at three levels of APOE4-related genetic risk for sporadic AD (APOE4/4 n = 19, APOE3/4 n = 32 or non-carriers n = 37). Concentrations of plasma p-tau181, p-tau231 and GFAP were measured using Single molecule array (Simoa), regional AS deposition with 11C-PiB positron emission tomography (PET), and cognitive performance with a preclinical composite. Significant differences in plasma p-tau181 and p-tau231, but not plasma GFAP concentrations were present between the APOE4 gene doses, explained solely by brain AS load. All plasma biomarkers correlated positively with AS PET in the total study population. This correlation was driven by APOE3/3 carriers for plasma p-tau markers and APOE4/4 carriers for plasma GFAP. Voxel-wise associations with amyloid-PET revealed different spatial patterns for plasma p-tau markers and plasma GFAP. Only higher plasma GFAP correlated with lower cognitive scores. Our observations suggest that plasma p-tau and plasma GFAP are both early AD markers reflecting different AS-related processes. Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional β-amyloid (Aβ) pathology and cognitive performance head-to-head in clinically unimpaired elderly (n = 88) at three levels of APOE4-related genetic risk for sporadic AD (APOE4/4 n = 19, APOE3/4 n = 32 or non-carriers n = 37). Concentrations of plasma p-tau181, p-tau231 and GFAP were measured using Single molecule array (Simoa), regional Aβ deposition with 11C-PiB positron emission tomography (PET), and cognitive performance with a preclinical composite. Significant differences in plasma p-tau181 and p-tau231, but not plasma GFAP concentrations were present between the APOE4 gene doses, explained solely by brain Aβ load. All plasma biomarkers correlated positively with Aβ PET in the total study population. This correlation was driven by APOE3/3 carriers for plasma p-tau markers and APOE4/4 carriers for plasma GFAP. Voxel-wise associations with amyloid-PET revealed different spatial patterns for plasma p-tau markers and plasma GFAP. Only higher plasma GFAP correlated with lower cognitive scores. Our observations suggest that plasma p-tau and plasma GFAP are both early AD markers reflecting different Aβ-related processes. Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we compared the biomarker levels and their association with regional β-amyloid (Aβ) pathology and cognitive performance head-to-head in clinically unimpaired elderly (n = 88) at three levels of APOE4-related genetic risk for sporadic AD (APOE4/4 n = 19, APOE3/4 n = 32 or non-carriers n = 37). Concentrations of plasma p-tau181, p-tau231 and GFAP were measured using Single molecule array (Simoa), regional Aβ deposition with C-PiB positron emission tomography (PET), and cognitive performance with a preclinical composite. Significant differences in plasma p-tau181 and p-tau231, but not plasma GFAP concentrations were present between the APOE4 gene doses, explained solely by brain Aβ load. All plasma biomarkers correlated positively with Aβ PET in the total study population. This correlation was driven by APOE3/3 carriers for plasma p-tau markers and APOE4/4 carriers for plasma GFAP. Voxel-wise associations with amyloid-PET revealed different spatial patterns for plasma p-tau markers and plasma GFAP. Only higher plasma GFAP correlated with lower cognitive scores. Our observations suggest that plasma p-tau and plasma GFAP are both early AD markers reflecting different Aβ-related processes. |
ArticleNumber | 106175 |
Author | Koivumäki, Mikko Lantero-Rodriguez, Juan Karrasch, Mira Pietilä, Elina Snellman, Anniina Helin, Semi Zetterberg, Henrik Blennow, Kaj Rinne, Juha O. Karikari, Thomas K. Ekblad, Laura L. Ashton, Nicholas J. |
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CitedBy_id | crossref_primary_10_1016_j_arr_2024_102290 crossref_primary_10_1093_arclin_acae019 crossref_primary_10_1007_s11357_024_01130_2 crossref_primary_10_3233_JAD_230823 crossref_primary_10_3390_biom14010093 crossref_primary_10_1002_alz_13804 crossref_primary_10_3390_neurolint15040092 |
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Keywords | Biomarker AD CNS P-tau181 Simoa p-tau GFAP Blood biomarkers P-tau231 beta-amyloid APCC Aβ VOI Apolipoprotein E MMSE CSF SUVR Preclinical APOE Alzheimer's disease PET |
Language | English |
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143 Langbaum (10.1016/j.nbd.2023.106175_bb0145) 2020 Mielke (10.1016/j.nbd.2023.106175_bb0170) 2018 Karikari (10.1016/j.nbd.2023.106175_bb0130) 2022 Meyer (10.1016/j.nbd.2023.106175_bb0165) 2022; 91 Randolph (10.1016/j.nbd.2023.106175_bb0210) 1998; 20 Kanmert (10.1016/j.nbd.2023.106175_bb0115) 2015 Ashton (10.1016/j.nbd.2023.106175_bb0020) 2021; 141 Cicognola (10.1016/j.nbd.2023.106175_bb0065) 2021 Jack (10.1016/j.nbd.2023.106175_bb0105) 2018 Karikari (10.1016/j.nbd.2023.106175_bb0120) 2020; 19 Chatterjee (10.1016/j.nbd.2023.106175_bb0050) 2021 Pereira (10.1016/j.nbd.2023.106175_bb0195) 2021; 144 Sato (10.1016/j.nbd.2023.106175_bb0220) 2018; 97 Toppala (10.1016/j.nbd.2023.106175_bb0255) 2021; 96 Moscoso (10.1016/j.nbd.2023.106175_bb0180) 2021 Pontecorvo (10.1016/j.nbd.2023.106175_bb0200) 2022; 79 Baiardi (10.1016/j.nbd.2023.106175_bb0035) 2022 Snellman (10.1016/j.nbd.2023.106175_bb0230) 2022 Karikari (10.1016/j.nbd.2023.106175_bb0125) 2021; 26 Suárez-Calvet (10.1016/j.nbd.2023.106175_bb0245) 2020 |
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Neurol. contributor: fullname: Karikari – volume: 141 year: 2021 ident: 10.1016/j.nbd.2023.106175_bb0020 article-title: Plasma p-tau231: a new biomarker for incipient Alzheimer’s disease pathology publication-title: Acta Neuropathol. doi: 10.1007/s00401-021-02275-6 contributor: fullname: Ashton – start-page: 78 year: 2021 ident: 10.1016/j.nbd.2023.106175_bb0045 article-title: Differences between plasma and cerebrospinal fluid glial fibrillary acidic protein levels across the Alzheimer disease continuum publication-title: JAMA Neurol. contributor: fullname: Benedet – volume: 16 year: 2020 ident: 10.1016/j.nbd.2023.106175_bb0090 article-title: Plasma biomarkers of astrocytic and neuronal dysfunction in early- and late-onset Alzheimer’s disease publication-title: Alzheimer’s & Dement.: J. Alzheimer’s Assoc. doi: 10.1016/j.jalz.2019.09.004 contributor: fullname: Elahi – volume: 19 start-page: 25 issue: 1 year: 2022 ident: 10.1016/j.nbd.2023.106175_bb0240 article-title: Association of plasma biomarkers, p-tau181, glial fibrillary acidic protein, and neurofilament light, with intermediate and long-term clinical Alzheimer’s disease risk: results from a prospective cohort followed over 17 years publication-title: Alzheimer’s & Dement.: J. Alzheimer’s Assoc. doi: 10.1002/alz.12614 contributor: fullname: Stocker – volume: 143 year: 2020 ident: 10.1016/j.nbd.2023.106175_bb0160 article-title: Longitudinal plasma p-tau217 is increased in early stages of Alzheimer’s disease publication-title: Brain J. Neurol. doi: 10.1093/brain/awaa286 contributor: fullname: Mattsson-Carlgren – volume: 78 year: 2020 ident: 10.1016/j.nbd.2023.106175_bb0030 article-title: Plasma glial fibrillary acidic protein levels differ along the spectra of amyloid burden and clinical disease stage publication-title: J. Alzheimer’s Dis.: JAD contributor: fullname: Asken – volume: 146 start-page: 1592 issue: 4 year: 2022 ident: 10.1016/j.nbd.2023.106175_bb0110 article-title: Head-to-head comparison of 10 plasma phospho-tau assays in prodromal Alzheimer’s disease publication-title: Brain doi: 10.1093/brain/awac333 contributor: fullname: Janelidze – start-page: 13 year: 2021 ident: 10.1016/j.nbd.2023.106175_bb0040 article-title: Clinical and analytical comparison of six Simoa assays for plasma P-tau isoforms P-tau181, P-tau217, and P-tau231 publication-title: Alzheimers Res. 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Snippet | Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. Here, we... |
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SubjectTerms | Aged Alzheimer Disease - diagnostic imaging Alzheimer Disease - genetics Alzheimer's disease Amyloid beta-Peptides APOE Apolipoprotein E Apolipoprotein E3 Apolipoprotein E4 - genetics beta-amyloid Biomarker Biomarkers Blood biomarkers Cognitive Dysfunction - diagnostic imaging Cognitive Dysfunction - genetics GFAP Glial Fibrillary Acidic Protein Humans Neurosciences Neurovetenskaper P-tau181 P-tau231 Preclinical tau Proteins |
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Title | Head-to-head comparison of plasma p-tau181, p-tau231 and glial fibrillary acidic protein in clinically unimpaired elderly with three levels of APOE4-related risk for Alzheimer's disease |
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