Circulating manganese superoxide dismutase (Mn-SOD, SOD 2) levels and its Ala16Val polymorphism in patients with Alzheimer's disease Alzheimer hastaliǧi'nda serum mangan superoksd dismutaz (MnSOD, SOD 2) enzim düzeyleri ve Ala16Val gen polimorfizmi

Kilinç E., Var A., MAVİOĞLU H., Dinç G., Karaçam M., Güvenç Y.

Turk Geriatri Dergisi, cilt.15, sa.1, ss.1-6, 2012 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 15 Sayı: 1
  • Basım Tarihi: 2012
  • Dergi Adı: Turk Geriatri Dergisi
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Social Sciences Citation Index (SSCI), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.1-6
  • Anahtar Kelimeler: Alzheimer disease, Genetic, Polymorphism, Superoxide dismutase
  • Manisa Celal Bayar Üniversitesi Adresli: Evet

Özet

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.