Affiliations: [a] Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), University of Piemonte Orientale, Novara, Italy
| [b] Immuno-Rheumatology Unit, Azienda Ospedaliero-Universitaria Maggiore della Carità, Novara, Italy
| [c] Department of Translational Medicine, Internal Medicine, University of Piemonte Orientale, Novara, Italy
| [d] Department Molecular Neurogenetics, Center for Molecular Neurobiology (ZMNH), University of Hamburg Medical Center (UKE), Hamburg, Germany
| [e] Department of Translational Medicine, Neurology Unit, University of Piemonte Orientale, Novara, Italy
| [f] Department of Pathophysiology and Transplantation, Neurology Unit, University of Milan, Fondazione Ca’ Granda, IRCCS Ospedale Policlinico, Milan, Italy
Correspondence:
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Correspondence to: Cristoforo Comi, MD, PhD, Department of Translational Medicine, University of Piemonte Orientale, Via Solaroli 17 - 28100 Novara, Italy. Tel.: +39 0321 3733965; Fax: +39 0321 3733298; E-mail: [email protected].
Abstract: Growth arrest specific 6 (Gas6) has neurotrophic and neuroinflammatory functions, and may play a role in Alzheimer’s disease (AD). In keeping with this hypothesis, we observed that cerebrospinal fluid (CSF) Gas6 is increased in AD patients compared to controls (63 versus 67 subjects; median value 13.3 versus 9.1 ng/ml; p < 0.0001). Thereafter, we assessed whether CSF Gas6 concentration was correlated to the following parameters: disease duration, MMSE score two years after clinical diagnosis, AD CSF biomarkers, and years of formal schooling. We detected an inverse correlation between CSF Gas6 levels at diagnosis and both disease duration (p < 0.0001) and decrease in the MMSE score two years later (p < 0.0001). Conversely, we found no correlation between CSF Gas6 and both AD biomarkers and years of formal schooling. In conclusion, our results suggest that upregulation of CSF Gas6 may be part of a defensive response aimed at counteracting AD progression.
