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Progression from mild to pronounced MCI is not associated with cerebrospinal fluid biomarker deviations.

Journal article
Authors Anders Wallin
Mattias Göthlin
Henrik Zetterberg
Carl Eckerström
Kaj Blennow
Åke Edman
Karin Lind
Arto Nordlund
Sindre Rolstad
Marie Gustavsson
Published in Dementia and geriatric cognitive disorders
Volume 32
Issue 3
Pages 193-7
ISSN 1421-9824
Publication year 2011
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 193-7
Language en
Links dx.doi.org/10.1159/000333034
Keywords Aged, Alzheimer Disease, cerebrospinal fluid, psychology, Amyloid beta-Peptides, cerebrospinal fluid, Apolipoproteins E, blood, Biological Markers, cerebrospinal fluid, Dementia, cerebrospinal fluid, psychology, Disease Progression, Educational Status, Electroencephalography, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Mild Cognitive Impairment, cerebrospinal fluid, psychology, Neurofilament Proteins, cerebrospinal fluid, Neuropsychological Tests, Peptide Fragments, cerebrospinal fluid, Tomography, Emission-Computed, Single-Photon, tau Proteins, cerebrospinal fluid
Subject categories Psychiatry

Abstract

Background/Aim: Detection of cerebrospinal fluid (CSF) biomarker deviations improve prediction of progression from mild cognitive impairment (MCI) to dementia. However, it is not settled whether the same pattern exists in patients progressing from very mild to more pronounced MCI. Given that neurodegenerative processes occur very early in the disease course, we also expected to find biomarker deviations in these patients. Methods: A total of 246 memory clinic patients with non-progressive (n = 161), progressive (n = 19), or converting (n = 66) MCI, 67 with stable dementia, and 80 controls were followed for 24 months. At baseline, CSF total tau (T-tau), β-amyloid 1–42 (Aβ42) and the light subunit of neurofilament protein (NFL) were determined. Results: Patients with converting MCI and stable dementia had lower CSF Aβ42 concentrations and higher T-tau concentrations and NFL in comparison with controls and non-progressive/progressive MCI (p < 0.0005). No differences were found between progressive and non-progressive MCI. Conclusion: As expected, biomarker deviations predicted progression from MCI to dementia. Contrary to our hypothesis, progression from very mild MCI to more pronounced MCI was not reflected by biomarker deviations. The results suggest that the measured biomarkers are not early disease markers, or alternatively Alzheimer or vascular pathology is not the underlying cause in this patient group.

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