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A Novel ELISA for the Measurement of Cerebrospinal Fluid SNAP-25 in Patients with Alzheimer's Disease.

Journal article
Authors Annika Öhrfelt
Ann Brinkmalm
Julien Dumurgier
Henrik Zetterberg
Elodie Bouaziz-Amar
Jacques Hugon
Claire Paquet
Kaj Blennow
Published in Neuroscience
ISSN 1873-7544
Publication year 2018
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Language en
Links dx.doi.org/10.1016/j.neuroscience.2...
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Neurochemistry

Abstract

Synaptic degeneration is central in Alzheimer's disease (AD) pathogenesis and biomarkers to monitor this pathophysiology in living patients are warranted. We developed a novel sandwich enzyme-linked immunosorbent assay (ELISA) for the measurement of the pre-synaptic protein SNAP-25 in cerebrospinal fluid (CSF) and evaluated it as a biomarker for AD. CSF samples included a pilot study consisting of AD (N = 26) and controls (N = 26), and two independent clinical cohorts of AD patients and controls. Cohort I included CSF samples from patients with dementia due to AD (N = 17), patients with mild cognitive impairment (MCI) due to AD (N = 5) and controls (N = 17), and cohort II CSF samples from patients with dementia due to AD (N = 24), patients with MCI due to AD (N = 18) and controls (N = 36). CSF levels of SNAP-25 were significantly increased in patients with AD compared with controls (P ≤ 0.00001). In both clinical cohorts, CSF levels of SNAP-25 were significantly increased in patients with MCI due to AD (P < 0.0001). SNAP-25 could differentiate dementia due to AD (N = 41) from controls (N = 52) and MCI due to AD (N = 23) from controls (N = 52) with areas under the curve of 0.967 (P < 0.0001) and 0.948 (P < 0.0001), respectively. CSF SNAP-25 is a promising AD biomarker that differentiates AD patients in different clinical stages of the disease from controls with excellent diagnostic accuracy. Future studies should address the specificity of the CSF SNAP-25 against common differential diagnoses to AD, as well as how the biomarker changes in response to treatment with disease-modifying drug candidates.

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