Cerebrospinal Fluid and Plasma Biomarkers do not Differ in the Presenile and Late-Onset Behavioral Variants of Frontotemporal Dementia.


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: 23 2 2020
medline: 20 4 2021
entrez: 22 2 2020
Statut: ppublish

Résumé

Memory troubles and hippocampal atrophy are considered more frequent and focal atrophy less severe in late-onset (>65 years) than in presenile behavioral variant of frontotemporal dementia (bvFTD). To compare cerebrospinal fluid (CSF) and plasma biomarkers in late-onset and presenile bvFTD. Multicentric retrospective study (2007-2017) on patients with clinical diagnosis of bvFTD. This study included 44 patients (67%) with presenile and 22 (33%) with late-onset bvFTD (comparable mean disease duration; n = 11 with causal mutations). Hippocampal atrophy was more frequent (80% versus 25.8%) and severe in late-onset bvFTD (median Scheltens score: 3 [0-4] versus 1 [0-3]), without difference after adjustment for age. Lobar atrophy and focal hypometabolism/hypoperfusion were not different between groups. The median CSF Aβ1-42 and phosphorylated tau (P-tau) concentrations were in the normal range and comparable between groups. Axonal neurodegeneration biomarkers were within the normal range (CSF T-tau; plasma T-tau in late-onset bvFTD) or higher (plasma neurofilament light chain (NFL); plasma T-tau in presenile bvFTD) than the normal values, but globally not different between bvFTD groups. Plasma glial fibrillary acid protein (GFAP) was strongly increased in both bvFTD groups compared with the values in controls of the same age. The CSF and plasma biomarker profiles did not suggest a more aggressive neurodegeneration in the presenile group (comparable T-tau, NFL, and GFAP levels) or the co-existence of Alzheimer's disease in the late-onset group (comparable and within normal range CSF Aβ1-42 and P-tau). The severity of the neurodegenerative process seems comparable in presenile and late-onset bvFTD.

Sections du résumé

BACKGROUND
Memory troubles and hippocampal atrophy are considered more frequent and focal atrophy less severe in late-onset (>65 years) than in presenile behavioral variant of frontotemporal dementia (bvFTD).
OBJECTIVE
To compare cerebrospinal fluid (CSF) and plasma biomarkers in late-onset and presenile bvFTD.
METHODS
Multicentric retrospective study (2007-2017) on patients with clinical diagnosis of bvFTD.
RESULTS
This study included 44 patients (67%) with presenile and 22 (33%) with late-onset bvFTD (comparable mean disease duration; n = 11 with causal mutations). Hippocampal atrophy was more frequent (80% versus 25.8%) and severe in late-onset bvFTD (median Scheltens score: 3 [0-4] versus 1 [0-3]), without difference after adjustment for age. Lobar atrophy and focal hypometabolism/hypoperfusion were not different between groups. The median CSF Aβ1-42 and phosphorylated tau (P-tau) concentrations were in the normal range and comparable between groups. Axonal neurodegeneration biomarkers were within the normal range (CSF T-tau; plasma T-tau in late-onset bvFTD) or higher (plasma neurofilament light chain (NFL); plasma T-tau in presenile bvFTD) than the normal values, but globally not different between bvFTD groups. Plasma glial fibrillary acid protein (GFAP) was strongly increased in both bvFTD groups compared with the values in controls of the same age.
CONCLUSION
The CSF and plasma biomarker profiles did not suggest a more aggressive neurodegeneration in the presenile group (comparable T-tau, NFL, and GFAP levels) or the co-existence of Alzheimer's disease in the late-onset group (comparable and within normal range CSF Aβ1-42 and P-tau). The severity of the neurodegenerative process seems comparable in presenile and late-onset bvFTD.

Identifiants

pubmed: 32083577
pii: JAD190378
doi: 10.3233/JAD-190378
doi:

Substances chimiques

Amyloid beta-Peptides 0
Biomarkers 0
GFAP protein, human 0
Glial Fibrillary Acidic Protein 0
MAPT protein, human 0
Peptide Fragments 0
amyloid beta-protein (1-42) 0
tau Proteins 0

Types de publication

Journal Article Multicenter Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

903-911

Auteurs

Cecilia Marelli (C)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.
Inserm U1198 MMDN, Montpellier, France; EPHE, Paris, France, Montpellier, France.

Claire Hourregue (C)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.

Laure-Anne Gutierrez (LA)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.
INSERM U1061, Univ Montpellier, Neuropsychiatry: Epidemiological and Clinical Research, Montpellier, France.

Claire Paquet (C)

Center of Cognitive Neurology, Lariboisière Fernand-Widal Hospital, APHP, University of Paris Diderot, Paris, France.

Nicolas Menjot de Champfleur (N)

Institut d'Imagerie Fonctionnelle Humaine, I2FH, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.
Department of Neuroradiology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.
Team "Plasticity of Central Nervous System, Stem Cells and Glial Tumors, " Institut National de la Santé et de la Recherche Médicale Unité 583, Institut of Neurosciences of Montpellier, Saint Eloi Hospital, Montpellier, France.

Delphine De Verbizier (D)

Department of Nuclear Medicine, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.

Melissa Jacob (M)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.

Jonathan Dubois (J)

INSERM U1061, Univ Montpellier, Neuropsychiatry: Epidemiological and Clinical Research, Montpellier, France.

Aleksandra Maceski Maleska (AM)

Laboratoire de Biochimie Protéomique Clinique, INSERM-UM 1183, University Hospital Center, University of Montpellier, Montpellier, France.

Christophe Hirtz (C)

Laboratoire de Biochimie Protéomique Clinique, INSERM-UM 1183, University Hospital Center, University of Montpellier, Montpellier, France.

Sophie Navucet (S)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.

Karim Bennys (K)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.

Julien Dumurgier (J)

Center of Cognitive Neurology, Lariboisière Fernand-Widal Hospital, APHP, University of Paris Diderot, Paris, France.

Emmanuel Cognat (E)

Center of Cognitive Neurology, Lariboisière Fernand-Widal Hospital, APHP, University of Paris Diderot, Paris, France.

Claudine Berr (C)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.
INSERM U1061, Univ Montpellier, Neuropsychiatry: Epidemiological and Clinical Research, Montpellier, France.

Eloi Magnin (E)

Department of Neurology, Centre Mémoire Ressources Recherche Besançon Franche-Comté, CHU de Besançon, Besançon, France.

Sylvain Lehmann (S)

Laboratoire de Biochimie Protéomique Clinique, INSERM-UM 1183, University Hospital Center, University of Montpellier, Montpellier, France.

Audrey Gabelle (A)

Memory Research and Resources Alzheimer Center, Department of Neurology, University Hospital Center, Gui de Chauliac Hospital, Montpellier, France.
INSERM U1061, Univ Montpellier, Neuropsychiatry: Epidemiological and Clinical Research, Montpellier, France.

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Classifications MeSH