Cited by 156Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsCerebrospinal fluid and hydrocephalus

Glial fibrillar acidic protein in the cerebrospinal fluid of Alzheimer’s disease, dementia with Lewy bodies, and frontotemporal lobar degeneration

Ishiki, Aiko, Kamada, Maki, Kawamura, Yuki, Terao, Chiaki, Shimoda, Fumiko, Tomita, Naoki, Arai, Hiroyuki, Furukawa, Katsutoshi·2016·Journal of Neurochemistry

Abstract

Biomarkers in the cerebrospinal fluid (CSF) are currently regarded as indispensable indicators for accurate differential diagnosis of neurodegenerative disorders. Although high levels of astrocyte-secreted glial fibrillar acidic protein (GFAP) in the CSF of patients with Alzheimer's disease (AD) have been reported, the levels of GFAP in the CSF have not been fully investigated in other neurological disorders that cause dementia, such as dementia with Lewy bodies (DLB) and frontotemporal lobar degeneration (FTLD). In this study, we determined the levels of GFAP in the CSF of healthy control subjects and AD, DLB, and FTLD patients to address two questions: (i) Do the levels of GFAP differ among these disorders? and (ii) Can GFAP be used as a biomarker for the differential diagnosis of these neurodegenerative disorders? The levels of GFAP in AD, DLB, and FTLD patients were significantly higher than those in the healthy control subjects. Although the levels of GFAP were not significantly different between AD and DLB patients, a higher level of GFAP was observed in FTLD patients than in AD and DLB patients. It is concluded that representative neurological disorders causing dementia were associated with higher levels of GFAP in the CSF. We propose the following mechanism concerning the amount of glial fibrillar acidic protein (GFAP) in the cerebrospinal fluid (CSF) in Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and frontotemporal lobar degeneration (FTLD). The increase in the release of GFAP into CSF is considered to reflect the sum of degeneration of astrocytes and astrocytosis. The sum of degeneration and astrocytosis or the GFAP release could be in the order of FTLD > DLB > AD > normal condition.

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Crossref · 10.1111/jnc.13399

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Authors
Ishiki, A., Kamada, M., Kawamura, Y., Terao, C., Shimoda, F., Tomita, N., Arai, H., & Furukawa, K.
Affiliations
Tohoku University (JP)
Corresponding author
Furukawa, Katsutoshi
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2015-11-11
Volume
136
Issue
2
Pages
258-261
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W2134303321
Cited by
156
References
10
Citations by year
2026: 10 · 2025: 18 · 2024: 21 · 2023: 18 · 2022: 21 · 2021: 30 · 2020: 17 · 2019: 8 · 2018: 7 · 2017: 3 · 2016: 2
FWCI
3.25
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ministry of Health, Labour and Welfare
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
Keywords
glial fibrillary acidic protein, cerebrospinal fluid biomarkers, Alzheimer's disease, dementia with Lewy bodies, frontotemporal lobar degeneration, differential diagnosis of dementia, astrocyte activation, astrocyte degeneration
MeSH terms
Aged, Alzheimer Disease, Analysis of Variance, Female, Glial Fibrillary Acidic Protein, Humans, Male, Mental Status Schedule, Peptide Fragments, Amyloid beta-Peptides, tau Proteins, Lewy Body Disease, Frontotemporal Lobar Degeneration

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