Affiliations: [a] Reference Center for Biological Markers of Dementia (BIODEM), Laboratory of Neurochemistry and Behavior, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium | [b] Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB, Antwerp, Belgium | [c] Laboratory of Neurogenetics, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium | [d] Biobank, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium | [e] Department of Neurology and Memory Clinic, Hospital Network Antwerp (ZNA), Middelheim and Hoge Beuken, Antwerp, Belgium
Correspondence:
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Correspondence to: Prof. Dr. S. Engelborghs, Reference Center for Biological Markers of Dementia (BIODEM), University of Antwerp, Universiteitsplein 1, 2610 Antwerp, Belgium. Tel.: +32 32652394; Fax: +32 32652618; E-mail: sebastiaan.engelborghs@ua.ac.be.
Note: [1] These authors contributed equally to this manuscript.
Abstract: A significant proportion of patients with dementia with Lewy bodies (DLB) show Alzheimer's disease (AD) pathology like senile plaques and neurofibrillary tangles. Biomarkers in cerebrospinal fluid (CSF), such as amyloid-β1-42 (Aβ1-42), total tau (T-tau), and hyperphosphorylated tau (P-tau181P), are linked to the different pathological hallmarks of AD. We set up a study to investigate the influence of AD co-pathology on CSF biomarker concentrations and profiles in autopsy-confirmed DLB. DLB patients with senile plaques showed significantly lower CSF Aβ1-42 concentrations than DLB patients without senile plaques, but not compared to the AD patients. There were no significant differences in CSF T-tau or P-tau181P concentrations between DLB patients with and without neurofibrillary tangles. A correlation was found between the number of APOE ε4 alleles and Aβ1-42 CSF levels in DLB patients with senile plaques. Although the CSF biomarkers Aβ1-42, T-tau, and P-tau181P have an added diagnostic value for the differential dementia diagnosis, concomitant amyloid pathology in DLB limits the use of CSF Aβ1-42 for the differential diagnosis of AD versus DLB.
