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CSF biomarkers distinguish idiopathic normal pressure hydrocephalus from its mimics

Artikel i vetenskaplig tidskrift
Författare Anna Jeppsson
Carsten Wikkelsö
Kaj Blennow
Henrik Zetterberg
Radu Constantinescu
A. M. Remes
S. K. Herukka
T. Rauramaa
K. Nagga
V. Leinonen
Mats Tullberg
Publicerad i Journal of Neurology, Neurosurgery and Psychiatry
Volym 90
Nummer/häfte 10
Sidor 1117-1123
ISSN 0022-3050
Publiceringsår 2019
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap
Sidor 1117-1123
Språk en
Länkar dx.doi.org/10.1136/jnnp-2019-320826
Ämnesord Alzheimer's disease, biomarkers, corticobasal degeneration, CSF, frontotemporal dementia, idiopathic normal pressure hydrocephalus, Multiple systems atrophy, Parkinson's disease, Progressive supranuclear palsy, vascular dementia
Ämneskategorier Neurovetenskaper

Sammanfattning

Objective: To examine the differential diagnostic significance of cerebrospinal fluid (CSF) biomarkers reflecting Alzheimer's disease-related amyloid β (Aβ) production and aggregation, cortical neuronal damage, tau pathology, damage to long myelinated axons and astrocyte activation, which hypothetically separates patients with idiopathic normal pressure hydrocephalus (iNPH) from patients with other neurodegenerative disorders. Methods: The study included lumbar CSF samples from 82 patients with iNPH, 75 with vascular dementia, 70 with Parkinson's disease, 34 with multiple system atrophy, 34 with progressive supranuclear palsy, 15 with corticobasal degeneration, 50 with Alzheimer's disease, 19 with frontotemporal lobar degeneration and 54 healthy individuals (HIs). We analysed soluble amyloid precursor protein alpha (sAPPα) and beta (sAPPβ), Aβ species (Aβ38, Aβ40 and Aβ42), total tau (T-tau), phosphorylated tau, neurofilament light and monocyte chemoattractant protein 1 (MCP-1). Results: Patients with iNPH had lower concentrations of tau and APP-derived proteins in combination with elevated MCP-1 compared with HI and the non-iNPH disorders. T-tau, Aβ40 and MCP-1 together yielded an area under the curve of 0.86, differentiating iNPH from the other disorders. A prediction algorithm consisting of T-tau, Aβ40 and MCP-1 was designed as a diagnostic tool using CSF biomarkers. Conclusions: The combination of the CSF biomarkers T-tau, Aβ40 and MCP-1 separates iNPH from cognitive and movement disorders with good diagnostic sensitivity and specificity. This may have important implications for diagnosis and clinical research on disease mechanisms for iNPH. © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

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