Ani Kıçık1, Erdem Tüzün2, Emel Erdoğdu3, Başar Bılgıç4, Zeynep Tüfekçıoğlu4, Esin Öztürk-Işik5, Haşmet Hanağasi4, Hakan Gürvıt4. 1. Department of Physiology, Faculty of Medicine, Demiroğlu Bilim University, İstanbul, Turkey. 2. Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, İstanbul University, İstanbul, Turkey. 3. Hulusi Behçet Life Sciences Research Laboratory, Neuroimaging Unit, İstanbul University, İstanbul, Turkey. 4. Department of Neurology, Istanbul Faculty of Medicine, İstanbul University, İstanbul, Turkey. 5. Biomedical Engineering Institute, Boğaziçi University, İstanbul, Turkey.
Abstract
INTRODUCTION: Cognitive impairment is common in Parkinson's disease (PD) and PD patients with mild cognitive impairment (PD-MCI) are at increased risk of developing Parkinson's disease dementia (PDD). Reliable biomarkers are required for objective identification of cognitive decline in PD. In this pilot study, serum levels of well-known mediators of neuroinflammation were measured in PD patients with or without MCI to find out the involvement of neuroinflammation and microglial activation in PD-MCI. METHODS: 36 PD-MCI, 25 PD patients with normal cognition (PD-NC) and 19 healthy controls were recruited. Serum levels of NLR family pyrin domain containing 1 (NLRP1), NLRP3, caspase-1, NF-kB, IL-1b and IL-18 were measured by ELISA and a panel of neuropsychological tests was administered. RESULTS: PD-MCI patients showed significantly reduced levels of NF-kB, IL-1b and IL-18, whereas NLRP1, NLRP3 and caspase-1 levels were comparable among PD-NC and PD-MCI patients. IL-18 levels were positively correlated with Addenbrooke's Cognitive Examination-Revised and Symbol Digit Modalities Test scores. CONCLUSION: Levels of several microglial activation mediators are reduced in PD-MCI patients inferring a protective role to certain inflammation factors against cognitive decline in PD. Copyright:
INTRODUCTION: Cognitive impairment is common in Parkinson's disease (PD) and PD patients with mild cognitive impairment (PD-MCI) are at increased risk of developing Parkinson's disease dementia (PDD). Reliable biomarkers are required for objective identification of cognitive decline in PD. In this pilot study, serum levels of well-known mediators of neuroinflammation were measured in PD patients with or without MCI to find out the involvement of neuroinflammation and microglial activation in PD-MCI. METHODS: 36 PD-MCI, 25 PD patients with normal cognition (PD-NC) and 19 healthy controls were recruited. Serum levels of NLR family pyrin domain containing 1 (NLRP1), NLRP3, caspase-1, NF-kB, IL-1b and IL-18 were measured by ELISA and a panel of neuropsychological tests was administered. RESULTS: PD-MCI patients showed significantly reduced levels of NF-kB, IL-1b and IL-18, whereas NLRP1, NLRP3 and caspase-1 levels were comparable among PD-NC and PD-MCI patients. IL-18 levels were positively correlated with Addenbrooke's Cognitive Examination-Revised and Symbol Digit Modalities Test scores. CONCLUSION: Levels of several microglial activation mediators are reduced in PD-MCI patients inferring a protective role to certain inflammation factors against cognitive decline in PD. Copyright:
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