Affiliations: [a] Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Sweden
| [b] Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden
| [c] Department of Clinical Sciences, Clinical Memory Research Unit, Lund University, Sweden
| [d] Memory Clinic, Skåne University Hospital, Sweden
| [e] Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK
| [f]
UK Dementia Research Institute at UCL, London, UK
Correspondence:
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Correspondence to: Karolina Minta, Department of Psychiatry and Neurochemistry, Sahlgrenska University Hospital/Mölndal, S-431 80 Mölndal, Sweden. Tel.: +46735660741; E-mail: [email protected].
Abstract: Background:Brevican, neurocan, tenascin-C, and tenascin-R are extracellular matrix (ECM) proteins that are mainly expressed in the brain. They play important roles in proliferation and migration of neurons and other cell types in the brain. These ECM proteins may also be involved in various pathologies, including reactive gliosis. Objective:The aim of the study was to investigate if ECM protein concentrations in cerebrospinal fluid (CSF) are linked to the neurodegenerative process in Alzheimer’s disease (AD). Methods:Lumbar CSF samples from a non-AD control group (n = 50) and a clinically diagnosed AD group (n = 42), matched for age and gender, were analyzed using commercially available ELISAs detecting ECM proteins. Mann-Whitney U test was used to examine group differences, while Spearman’s rho test was used for correlations. Results:Brevican, neurocan, tenascin-R, and tenascin-C concentrations in AD patients did not differ compared to healthy controls or when the groups were dichotomized based on the Aβ42/40 cut-off. CSF tenascin-C and tenascin-R concentrations were significantly higher in women than in men in the AD group (p = 0.02). Conclusion:ECM proteins do not reflect AD-pathology in CSF. CSF tenascin-C and tenascin-R upregulation in women possibly reveal sexual dimorphism in the central nervous system immunity during AD.
