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DCLK-1 LEVEL IN MULTIPLE SCLEROSIS PATIENTS AND ITS CORRELATION WITH CLINIC.
Multiple Sclerosis and related Disorders 2020 May 23
INTRODUCTION AND OBJECTIVE: There are studies supporting the disruption of axonal transport in multiple sclerosis, a neurodegenerative disease. The aim of our study was to determine Doublecortin-like kinase 1 (DCLK1) levels in multiple sclerosis patients, which play a part in axonal transport, and to investigate its correlation with the disease.
MATERIALS AND METHODS: The study included 30 patients above 18 years of age with the diagnosis of multiple sclerosis and 30 healthy volunteers. The disease duration, number of annual attacks, Expanded Disability Status Scale (EDSS) scores and medications of the patients who had no history of attack within the last month were recorded. DCLK1 levels were studied in the venous blood samples taken from the patients and healthy volunteers using the ELISA method.
RESULTS: DCLK1 levels were significantly lower in the MS patient group than in the healthy control group. There was no significant correlation between disease duration, annual number of attacks, EDSS score and DCLK1 level.
CONCLUSION: Low levels of DCLK1 in multiple sclerosis patients support the disruption of axonal transport. The use of agents that provide DCLK1 expression may be a treatment option to prevent neurodegeneration in multiple sclerosis patients by eliminating the disruption in axonal transport, thereby improving the clinical course of the disease and cognition.
MATERIALS AND METHODS: The study included 30 patients above 18 years of age with the diagnosis of multiple sclerosis and 30 healthy volunteers. The disease duration, number of annual attacks, Expanded Disability Status Scale (EDSS) scores and medications of the patients who had no history of attack within the last month were recorded. DCLK1 levels were studied in the venous blood samples taken from the patients and healthy volunteers using the ELISA method.
RESULTS: DCLK1 levels were significantly lower in the MS patient group than in the healthy control group. There was no significant correlation between disease duration, annual number of attacks, EDSS score and DCLK1 level.
CONCLUSION: Low levels of DCLK1 in multiple sclerosis patients support the disruption of axonal transport. The use of agents that provide DCLK1 expression may be a treatment option to prevent neurodegeneration in multiple sclerosis patients by eliminating the disruption in axonal transport, thereby improving the clinical course of the disease and cognition.
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