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Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment

Cicognola, Claudia LU orcid ; Janelidze, Shorena LU ; Hertze, Joakim LU ; Zetterberg, Henrik LU ; Blennow, Kaj LU ; Mattsson-Carlgren, Niklas LU orcid and Hansson, Oskar LU orcid (2021) In Alzheimer's Research and Therapy 13(1).
Abstract

Introduction: Plasma glial fibrillary acidic protein (GFAP) is a marker of astroglial activation and astrocytosis. We assessed the ability of plasma GFAP to detect Alzheimer’s disease (AD) pathology in the form of AD-related amyloid-β (Aβ) pathology and conversion to AD dementia in a mild cognitive impairment (MCI) cohort. Method: One hundred sixty MCI patients were followed for 4.7 years (average). AD pathology was defined using cerebrospinal fluid (CSF) Aβ42/40 and Aβ42/total tau (T-tau). Plasma GFAP was measured at baseline and follow-up using Simoa technology. Results: Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72–0.86) and 0.80 (95% CI 0.72–0.86), respectively. When also... (More)

Introduction: Plasma glial fibrillary acidic protein (GFAP) is a marker of astroglial activation and astrocytosis. We assessed the ability of plasma GFAP to detect Alzheimer’s disease (AD) pathology in the form of AD-related amyloid-β (Aβ) pathology and conversion to AD dementia in a mild cognitive impairment (MCI) cohort. Method: One hundred sixty MCI patients were followed for 4.7 years (average). AD pathology was defined using cerebrospinal fluid (CSF) Aβ42/40 and Aβ42/total tau (T-tau). Plasma GFAP was measured at baseline and follow-up using Simoa technology. Results: Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72–0.86) and 0.80 (95% CI 0.72–0.86), respectively. When also including APOE ε4 status as a predictor, the accuracy of the model to detect abnormal CSF Aβ42/40 status improved (AUC = 0.86, p = 0.02). Plasma GFAP predicted subsequent conversion to AD dementia with an AUC of 0.84 (95% CI 0.77–0.91), which was not significantly improved when adding APOE ε4 or age as predictors to the model. Longitudinal GFAP slopes for Aβ-positive and MCI who progressed to dementia (AD or other) were significantly steeper than those for Aβ-negative (p = 0.007) and stable MCI (p < 0.0001), respectively. Conclusion: Plasma GFAP can detect AD pathology in patients with MCI and predict conversion to AD dementia.

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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Alzheimer’s disease, Blood biomarkers, GFAP, Mild cognitive impairment
in
Alzheimer's Research and Therapy
volume
13
issue
1
article number
68
publisher
BioMed Central (BMC)
external identifiers
  • scopus:85103559375
  • pmid:33773595
ISSN
1758-9193
DOI
10.1186/s13195-021-00804-9
language
English
LU publication?
yes
id
62f7d071-3028-42f9-9bf9-96936b2fe9fb
date added to LUP
2021-04-12 07:34:46
date last changed
2024-06-15 09:38:34
@article{62f7d071-3028-42f9-9bf9-96936b2fe9fb,
  abstract     = {{<p>Introduction: Plasma glial fibrillary acidic protein (GFAP) is a marker of astroglial activation and astrocytosis. We assessed the ability of plasma GFAP to detect Alzheimer’s disease (AD) pathology in the form of AD-related amyloid-β (Aβ) pathology and conversion to AD dementia in a mild cognitive impairment (MCI) cohort. Method: One hundred sixty MCI patients were followed for 4.7 years (average). AD pathology was defined using cerebrospinal fluid (CSF) Aβ42/40 and Aβ42/total tau (T-tau). Plasma GFAP was measured at baseline and follow-up using Simoa technology. Results: Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72–0.86) and 0.80 (95% CI 0.72–0.86), respectively. When also including APOE ε4 status as a predictor, the accuracy of the model to detect abnormal CSF Aβ42/40 status improved (AUC = 0.86, p = 0.02). Plasma GFAP predicted subsequent conversion to AD dementia with an AUC of 0.84 (95% CI 0.77–0.91), which was not significantly improved when adding APOE ε4 or age as predictors to the model. Longitudinal GFAP slopes for Aβ-positive and MCI who progressed to dementia (AD or other) were significantly steeper than those for Aβ-negative (p = 0.007) and stable MCI (p &lt; 0.0001), respectively. Conclusion: Plasma GFAP can detect AD pathology in patients with MCI and predict conversion to AD dementia.</p>}},
  author       = {{Cicognola, Claudia and Janelidze, Shorena and Hertze, Joakim and Zetterberg, Henrik and Blennow, Kaj and Mattsson-Carlgren, Niklas and Hansson, Oskar}},
  issn         = {{1758-9193}},
  keywords     = {{Alzheimer’s disease; Blood biomarkers; GFAP; Mild cognitive impairment}},
  language     = {{eng}},
  number       = {{1}},
  publisher    = {{BioMed Central (BMC)}},
  series       = {{Alzheimer's Research and Therapy}},
  title        = {{Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment}},
  url          = {{http://dx.doi.org/10.1186/s13195-021-00804-9}},
  doi          = {{10.1186/s13195-021-00804-9}},
  volume       = {{13}},
  year         = {{2021}},
}