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Published on: January 22, 2017
Heavy metal accumulation in Parkinson's disease: AN evaluation of hair analysis
Bekir Enes Demiryürek1, Seda Karayünlü Bozbaş2, Onur Gümüş2
1Department of Neurology, Faculty of Medicine, Istanbul Aydin University, Istanbul, Türkiye.
Background:
Heavy metals have been implicated in the pathophysiology of Parkinson's disease (PD) through mechanisms involving oxidative stress, mitochondrial dysfunction, neuroinflammation, and protein aggregation. However, the relationship between chronic metal accumulation and clinical severity remains incompletely understood.
Objective:
This case-control study investigated hair trace element concentrations and their associations with disease severity in patients with PD.
Methods:
Thirty-one patients with PD and 30 age- and sex-matched healthy controls were enrolled. Hair samples were analyzed using inductively coupled plasma optical emission spectrometry, and concentrations of multiple trace elements were determined. Clinical severity was assessed using the Movement Disorder Society-Unified Parkinson's Disease Rating Scale Part III (MDS-UPDRS III) and Hoehn and Yahr (H&Y) staging. Disease duration was also recorded.
Results:
There were no significant differences between groups regarding age or sex distribution. Hair aluminum concentrations were significantly lower in patients with PD, whereas zinc, nickel, and lead concentrations were significantly higher compared with controls (all p < 0.05). No significant between-group differences were observed for chromium, copper, iron, or manganese. Within the PD group, zinc demonstrated significant inverse correlations with MDS-UPDRS III scores (r = -0.53, p = 0.002), H&Y stage (r = -0.49, p = 0.005), and disease duration (r = -0.50, p = 0.004). No other trace element showed consistent associations with clinical measures.
Conclusions:
These findings suggest that zinc dysregulation is associated with greater disease severity and longer disease duration. Further longitudinal studies are needed to clarify the role of zinc homeostasis in Parkinson's disease.
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