Akash Roy1, Supriyo Choudhury2, Rebecca Banerjee3, Purba Basu4, Hrishikesh Kumar5. 1. Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India; Department of Physiology, University of Calcutta, Kolkata, India. Electronic address: akashachena25@gmail.com. 2. Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India. Electronic address: choudhurydrsupriyo@gmail.com. 3. Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India. Electronic address: rebeccabanerjee@yahoo.com. 4. Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India. Electronic address: poorva78@yahoo.co.in. 5. Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India. Electronic address: rishi_medicine@yahoo.com.
Abstract
INTRODUCTION: There is some evidence regarding the role of LAG-3, TLR mediated neuroinflammation in PD. METHODS: sLAG-3, TOLLIP, NLRP3 levels were measured in PD and healthy controls. RESULTS: These markers were significantly higher in PD and were associated with progression. CONCLUSION: sLAG3 and TOLLIP are involved in the NLRP3 mediated inflammatory activation in PD.
INTRODUCTION: There is some evidence regarding the role of LAG-3, TLR mediated neuroinflammation in PD. METHODS: sLAG-3, TOLLIP, NLRP3 levels were measured in PD and healthy controls. RESULTS: These markers were significantly higher in PD and were associated with progression. CONCLUSION: sLAG3 and TOLLIP are involved in the NLRP3 mediated inflammatory activation in PD.
Authors: Stephanie E A Burnell; Lorenzo Capitani; Bruce J MacLachlan; Georgina H Mason; Awen M Gallimore; Andrew Godkin Journal: Immunother Adv Date: 2021-12-20