Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration.


Journal

Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863

Informations de publication

Date de publication:
2020
Historique:
pubmed: 18 8 2020
medline: 10 9 2021
entrez: 18 8 2020
Statut: ppublish

Résumé

It is still unknown if serum glial fibrillary acidic protein (GFAP) is a useful marker in frontotemporal lobar degeneration (FTLD). To assess the diagnostic and prognostic value of serum GFAP in a large cohort of patients with FTLD. In this retrospective study, performed on 406 participants, we measured serum GFAP concentration with an ultrasensitive Single molecule array (Simoa) method in patients with FTLD, Alzheimer's disease (AD), and in cognitively unimpaired elderly controls. We assessed the role of GFAP as marker of disease severity by analyzing the correlation with clinical variables, neurophysiological data, and cross-sectional brain imaging. Moreover, we evaluated the role of serum GFAP as a prognostic marker of disease survival. We observed significantly higher levels of serum GFAP in patients with FTLD syndromes, except progressive supranuclear palsy, compared with healthy controls, but not compared with AD patients. In FTLD, serum GFAP levels correlated with measures of cognitive dysfunction and disease severity, and were associated with indirect measures of GABAergic deficit. Serum GFAP concentration was not a significant predictor of survival. Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD.

Sections du résumé

BACKGROUND
It is still unknown if serum glial fibrillary acidic protein (GFAP) is a useful marker in frontotemporal lobar degeneration (FTLD).
OBJECTIVE
To assess the diagnostic and prognostic value of serum GFAP in a large cohort of patients with FTLD.
METHODS
In this retrospective study, performed on 406 participants, we measured serum GFAP concentration with an ultrasensitive Single molecule array (Simoa) method in patients with FTLD, Alzheimer's disease (AD), and in cognitively unimpaired elderly controls. We assessed the role of GFAP as marker of disease severity by analyzing the correlation with clinical variables, neurophysiological data, and cross-sectional brain imaging. Moreover, we evaluated the role of serum GFAP as a prognostic marker of disease survival.
RESULTS
We observed significantly higher levels of serum GFAP in patients with FTLD syndromes, except progressive supranuclear palsy, compared with healthy controls, but not compared with AD patients. In FTLD, serum GFAP levels correlated with measures of cognitive dysfunction and disease severity, and were associated with indirect measures of GABAergic deficit. Serum GFAP concentration was not a significant predictor of survival.
CONCLUSION
Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD.

Identifiants

pubmed: 32804092
pii: JAD200608
doi: 10.3233/JAD-200608
doi:

Substances chimiques

Biomarkers 0
GFAP protein, human 0
Glial Fibrillary Acidic Protein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1129-1141

Auteurs

Alberto Benussi (A)

Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.

Nicholas J Ashton (NJ)

Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Mölndal, Sweden.
King's College London, Institute of Psychiatry, Psychology & Neuroscience, Maurice Wohl Clinical Neuroscience Institute, London, UK.
NIHR Biomedical Research Centre for Mental Health & Biomedical Research Unit for Dementia at South London & Maudsley NHS Foundation, London, UK.

Thomas K Karikari (TK)

Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.

Stefano Gazzina (S)

Neurophysiology Unit, ASST Spedali Civili, Brescia, Italy.

Enrico Premi (E)

Stroke Unit, ASST Spedali Civili, Brescia, Italy.

Luisa Benussi (L)

Molecular Markers Laboratory, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.

Roberta Ghidoni (R)

Molecular Markers Laboratory, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.

Juan Lantero Rodriguez (JL)

Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.

Andreja Emeršič (A)

Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Department of Neurology, University Medical Centre Ljubljana, Slovenia.

Giuliano Binetti (G)

MAC Memory Clinic and Molecular Markers Laboratory, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.

Silvia Fostinelli (S)

Molecular Markers Laboratory, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.

Marcello Giunta (M)

Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.

Roberto Gasparotti (R)

Neuroradiology Unit, University of Brescia, Brescia, Italy.

Henrik Zetterberg (H)

Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Department of Neurology, University Medical Centre Ljubljana, Slovenia.
UK Dementia Research Institute at UCL, London, UK.
Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.

Kaj Blennow (K)

Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Department of Neurology, University Medical Centre Ljubljana, Slovenia.

Barbara Borroni (B)

Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.

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