Annals of Clinical and Translational Neurology (Mar 2020)

Nonmercaptalbumin as an oxidative stress marker in Parkinson’s and PARK2 disease

  • Shin‐Ichi Ueno,
  • Taku Hatano,
  • Ayami Okuzumi,
  • Shinji Saiki,
  • Yutaka Oji,
  • Akio Mori,
  • Takahiro Koinuma,
  • Motoki Fujimaki,
  • Haruka Takeshige‐Amano,
  • Akihide Kondo,
  • Naoyuki Yoshikawa,
  • Takahiro Nojiri,
  • Makoto Kurano,
  • Keiko Yasukawa,
  • Yutaka Yatomi,
  • Hitoshi Ikeda,
  • Nobutaka Hattori

DOI
https://doi.org/10.1002/acn3.50990
Journal volume & issue
Vol. 7, no. 3
pp. 307 – 317

Abstract

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Abstract Objective To investigate the oxidized albumin ratio, which is the redox ratio of human nonmercaptalbumin (HNA) to serum albumin (%HNA), as a biomarker in idiopathic Parkinson’s disease (iPD) and related neurodegenerative disorders. Methods This prospective study enrolled 216 iPD patients, 15 patients with autosomal recessive familial PD due to parkin mutations (PARK2), 30 multiple system atrophy (MSA) patients, 32 progressive nuclear palsy (PSP) patients, and 143 healthy controls. HNA was analyzed using modified high‐performance liquid chromatography and was evaluated alongside other parameters. Results iPD and PARK2 patients had a higher %HNA than controls (iPD vs. controls: odds ratio (OR) 1.325, P < 0.001; PARK2 vs. controls: OR 1.712, P < 0.001). Even iPD patients at an early Hoehn & Yahr stage (I and II) showed a higher %HNA than controls. iPD patients had a higher %HNA than MSA and PSP patients (iPD vs. MSA: OR 1.249, P < 0.001, iPD vs. PSP: OR 1.288, P < 0.05). When discriminating iPD patients from controls, %HNA corrected by age achieved an AUC of 0.750; when discriminating iPD patients from MSA and PSP patients, an AUC of 0.747 was achieved. Furthermore, uric acid, an antioxidant compound, was decreased in iPD patients, similar to the change in %HNA. Interpretation %HNA was significantly increased in iPD and PARK2 patients compared with controls, regardless of disease course and severity. Oxidative stress might be increased from the early stages of iPD and PARK2 and play an important role in their pathomechanisms.