Journal of molecular neuroscience : MN · 2024
Lack of Association between BDNF rs6265 and Multiple Sclerosis: A Case-Control Study.
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Liampas Ioannis, Tsirelis Daniil, Dastamani Metaxia, Pariou Stavroula-Ioanna, Papasavva Maria, Katsarou Martha-Spyridoula, Tsolakou Annia, Tsatsakis Aristidis, Bogdanos Dimitrios P, Drakoulis Nikolaos, Dardiotis Efthimios, Siokas Vasileios
Аннотация
BACKGROUND AND OBJECTIVES: Data on the association between BDNF rs6265 and multiple sclerosis (MS) are scarce and heterogeneous.
MATERIALS AND METHODS: We undertook a case-control study design. Newly diagnosed individuals with MS based on the 2017 revision of the McDonald criteria were recruited from the Neurology Department of the General University Hospital of Larissa. Healthy controls with a free medical and family history were also recruited. The relationship between BDNF rs6265 and MS was defined as the primary outcome. The association between rs6265 and age of MS onset, spinal lesions, and clinical manifestations at the time of MS onset were defined as the secondary outcomes.
RESULTS: We genotyped a total of 200 patients with MS and 205 healthy controls, yielding a sample power of approximately 80%. BDNF rs6265 was in Hardy-Weinberg Equilibrium among healthy participants (p = 0.64). No significant relationship was revealed between rs6265 and MS [log-additive OR = 0.83 (0.57,1.21), over-dominant OR = 0.73 (0.48,1.14), recessive OR = 1.24 (0.37,4.12), dominant OR = 0.77 (0.50,1.17), co-dominant OR1 = 0.74 (0.48,1.14) and co-dominant OR2 = 1.13 (0.34,3.80)]. Additionally, rs6265 was unrelated to the age of MS onset according to both unadjusted and sex-adjusted cox-proportional models. Finally, rs6265 was not associated with the presence of spinal lesions (cervical or thoracic) at MS onset, according to both unadjusted and age and sex-adjusted logistic regression models.
CONCLUSIONS: We failed to establish an association between BDNF rs6265 and the risk of MS, the age of onset, the presence of spinal lesions, and the clinical manifestations at the onset.
MATERIALS AND METHODS: We undertook a case-control study design. Newly diagnosed individuals with MS based on the 2017 revision of the McDonald criteria were recruited from the Neurology Department of the General University Hospital of Larissa. Healthy controls with a free medical and family history were also recruited. The relationship between BDNF rs6265 and MS was defined as the primary outcome. The association between rs6265 and age of MS onset, spinal lesions, and clinical manifestations at the time of MS onset were defined as the secondary outcomes.
RESULTS: We genotyped a total of 200 patients with MS and 205 healthy controls, yielding a sample power of approximately 80%. BDNF rs6265 was in Hardy-Weinberg Equilibrium among healthy participants (p = 0.64). No significant relationship was revealed between rs6265 and MS [log-additive OR = 0.83 (0.57,1.21), over-dominant OR = 0.73 (0.48,1.14), recessive OR = 1.24 (0.37,4.12), dominant OR = 0.77 (0.50,1.17), co-dominant OR1 = 0.74 (0.48,1.14) and co-dominant OR2 = 1.13 (0.34,3.80)]. Additionally, rs6265 was unrelated to the age of MS onset according to both unadjusted and sex-adjusted cox-proportional models. Finally, rs6265 was not associated with the presence of spinal lesions (cervical or thoracic) at MS onset, according to both unadjusted and age and sex-adjusted logistic regression models.
CONCLUSIONS: We failed to establish an association between BDNF rs6265 and the risk of MS, the age of onset, the presence of spinal lesions, and the clinical manifestations at the onset.