2Celal Bayar Üniversitesi Tıp Fakültesi Nöroloji Anabilim Dalı MANİSA
3Celal Bayar Üniversitesi Tıp Fakültesi Halk Sağlığı Anabilim Dalı MANİSA
4Celal Bayar Üniversitesi Sağlık Hizmetleri Meslek Yüksekokulu, Biyokimya Bölümü MANİSA Introduction: Amyloid beta protein, DNA damage, oxygen free radicals and mitochondrial dysfunction are propounded mechanisms for pathogenesis of Alzheimer's disease (AD). In this study, we have focused on manganese superoxide dismutase (MnSOD, SOD-2), the most important scavenger enzyme in mitochondria. Ala16Val polymorphism, the most common variation in the SOD-2 gene, is considered to participate in the pathogenesis of neurodegenerative diseases. Therefore, in this study, we aimed to explain whether the MnSOD levels and its Ala16Val polymorphism are associated with Alzheimer's disease.
Materials and Method: We determined the protein SOD-2 levels and its Ala16Val polymorphism in patients with AD (n=55) and control samples (n=62) from age and sex matched healthy volunteers. Real time pcr and spectrophotometry were used for the analyses of Ala16Val polymorphism and SOD-2 levels respectively.
Results: We found significantly increased MnSOD levels in patients with Alzheimer's when compared to the healthy volunteers (144±67 U/gHb, 76±51 U/gHb respectively, p=0.001). But, there is no difference in Ala16Val polymorphism between the two groups.
Conclusion: We consider that MnSOD is a critical antioxidant enzyme for mitochondrial vitality in Alzheimer patients, but its polymorphic structure does not contribute to pathophysiology of Alzheimer's.
Keywords : Alzheimer Disease; Superoxide Dismutase; Polymorphism, Genetic