CSF sAPPß, YKL-40, and neurofilament light in frontotemporal lobar degeneration
| Autor: | Alcolea D., Vilaplana E., Suárez-Calvet M., Illán-Gala I., Blesa R., Clarimón J., Lladó A., Sánchez-Valle R., Molinuevo J.L., García-Ribas G., Compta Y., Martí M.J., Piñol-Ripoll G., Amer-Ferrer G., Noguera A., García-Martín A., Fortea J., Lleó A. |
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| Rok vydání: | 2017 |
| Předmět: |
frontal variant frontotemporal dementia
amyloid precursor protein neurofilament frontotemporal dementia tau protein Article male middle aged chitinase 3 like protein 1 neurofilament protein controlled study human neurofilament protein L nuclear magnetic resonance imaging cerebrospinal fluid analysis protein cerebrospinal fluid level neurofilament light protein neuroimaging amyloid beta protein[1-42] adult Mini Mental State Examination genetic screening progressive supranuclear palsy amyloid beta-protein (1-42) biological marker major clinical study unclassified drug clinical practice protein phosphorylation aged female priority journal peptide fragment semantic dementia amyloid beta protein progressive nonfluent aphasia cerebrospi diagnostic accuracy primary progressive aphasia diagnostic value disease duration Alzheimer disease cortical thickness (brain) corticobasal degeneration |
| Zdroj: | NEUROLOGY r-IIB SANT PAU. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica Sant Pau instname |
| ISSN: | 0028-3878 |
| Popis: | Objective: To analyze the clinical utility of 3 CSF biomarkers and their structural imaging correlates in a large cohort of patients with different dementia and parkinsonian syndromes within the spectrum of frontotemporal lobar degeneration (FTLD). Methods: We analyzed 3 CSF biomarkers (YKL-40, soluble ß fragment of amyloid precursor protein [sAPPß], neurofilament light [NfL]) and core Alzheimer disease (AD) biomarkers (ß-amyloid 1-42, total tau, phosphorylated tau) in patients with FTLD-related clinical syndromes (n = 159): behavioral variant of frontotemporal dementia (n = 68), nonfluent (n = 23) and semantic (n = 19) variants of primary progressive aphasia, progressive supranuclear palsy (n = 28), and corticobasal syndrome (n = 21). We also included patients with AD (n = 72) and cognitively normal controls (CN; n = 76). We compared cross-sectional biomarker levels between groups, studied their correlation with cortical thickness, and evaluated their potential diagnostic utility. Results: Patients with FTLD-related syndromes had lower levels of sAPPß than CN and patients with AD. The levels of sAPPß showed a strong correlation with cortical structural changes in frontal and cingulate areas. NfL and YKL-40 levels were high in both the FTLD and AD groups compared to controls. In the receiver operating characteristic analysis, the sAPPß/YKL-40 and NfL/sAPPß ratios had areas under the curve of 0.91 and 0.96, respectively, distinguishing patients with FTLD from CN, and of 0.84 and 0.85, distinguishing patients with FTLD from patients with AD. Conclusions: The combination of sAPPß with YKL-40 and with NfL in CSF could be useful to increase the certainty of the diagnosis of FTLD-related syndromes in clinical practice. Classification of evidence: This study provides Class III evidence that CSF levels of sAPPß, YKL-40, and NfL are useful to identify patients with FTLD-related syndromes. © 2017 American Academy of Neurology. |
| Databáze: | OpenAIRE |
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