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Clin Chem. 2018 Jun;64(6):927-937. doi: 10.1373/clinchem.2017.283028. Epub 2018 Mar 9.

Neurogranin as Cerebrospinal Fluid Biomarker for Alzheimer Disease: An Assay Comparison Study.

Author information

1
Neurochemistry laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, VU University Medical Center Amsterdam, the Netherlands; e.willemse@vumc.nl.
2
Alzheimer Center, Department of Neurology, Amsterdam Neuroscience, VU University Medical Center Amsterdam, the Netherlands.
3
Reference Center for Biological Markers of Dementia (BIODEM), Department of Biomedical Sciences, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium.
4
ADx NeuroSciences, Ghent, Belgium.
5
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.
6
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
7
VU University Medical Center, Epidemiology & Biostatistics, Amsterdam, the Netherlands.
8
UCL Institute of Neurology, Department of Molecular Neuroscience, Queen Square, London, United Kingdom.
9
UK Dementia Research Institute, London, United Kingdom.
10
Department of Neurology, Knight Alzheimer's Disease Research Center, Hope Center for Neurodegenerative Disorders, Washington University School of Medicine, St. Louis, MO.
11
Neurochemistry laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, VU University Medical Center Amsterdam, the Netherlands.

Abstract

BACKGROUND:

Neurogranin in cerebrospinal fluid (CSF) correlates with cognitive decline and is a potential novel biomarker for Alzheimer disease (AD) dementia. We investigated the analytical and diagnostic performance of 3 commonly used neurogranin assays in the same cohort of patients to improve the interpretability of CSF neurogranin test results.

METHODS:

The neurogranin Erenna® assay from Washington University, St. Louis, MO (WashU); ELISA from ADx Neurosciences; and ELISA from Gothenburg University, Mölndal, Sweden (UGot), were compared using silver staining and Western blot after gel electrophoresis. Clinical performance of the 3 assays was compared in samples from individuals diagnosed with subjective cognitive decline (n = 22), and in patients with AD (n = 22), frontotemporal dementia (n = 22), dementia with Lewy bodies (n = 22), or vascular dementia (n = 20), adjusted for sex and age.

RESULTS:

The assays detected different epitopes of neurogranin: the WashU assay detected the N-terminal part of neurogranin (S10-D23) and a C-terminal part (G49-G60), the ADx assay detected C-terminal neurogranin truncated at P75, and the UGot assay detected the C-terminal neurogranin with intact ending (D78). Spearman ρ was 0.95 between ADx and WashU, 0.87 between UGot and WashU, and 0.81 between UGot and ADx. ANCOVA (analysis of covariance) showed group differences for ranked neurogranin concentrations in each assay (all P < 0.05), with specific increases in AD.

CONCLUSIONS:

Although the 3 assays target different epitopes on neurogranin and have different calibrators, the high correlations and the similar group differences suggest that the different forms of neurogranin in CSF carry similar diagnostic information, at least in the context of neurodegenerative diseases.

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