Neutron Activation Analysis of Trace Elements in Parkinson’s Disease

Abstract

Relevance: Parkinson's disease along with secondary parkinsonism is the most common neurodegenerative disease of the elderly people and remains a serious medical and social problem. Parkinsonism
 or shaking palsy is categorized as a chronic progressive brain disease. Studying the trace elements imbalance, determining their content in bio-substrates, particularly in hair, is one of the methodological
 approaches for early diagnosis of the neurodegenerative processes and improving the methodology for
 effective treatment.
 Purpose: To investigate by neutron activation analysis the hair elemental composition of patients with
 secondary parkinsonism in chronic liver failure (SPCLF) and to assess the imbalance of trace elements
 affecting the severity and course of the disease.
 Material and methods: The study involved 77 patients aged 30 to 82 years, including 21 patients with
 parkinsonism syndrome in chronic liver failure, 29 patients with Parkinson's disease and 27 patients
 with vascular parkinsonism.The trace element status of patients was studied by hair analysis using the
 neutron activation method at the VVR-SM reactor of the INP.
 Results: The hair elemental composition of patients with secondary parkinsonism in chronic liver failure was studied and the content of copper, manganese, selenium, chromium, zinc, cobalt and bromine
 in the hair of all studied patients was determined. A comparative assessment of the elements imbalance in the studied groups was carried out. Correlation analysis between the elements revealed a positive correlation between manganese and iron (r =0.51) and a negative correlation between manganese
 and bromine (r =–0.74) in the group of patients with secondary parkinsonism in chronic liver failure.
 Conclusion: The imbalance of trace elements affecting the severity and course of the disease was assessed. It is shown that the revealed deficiency of copper, iron and zinc contribute to even greater accumulation of manganese in the basal ganglia, worsening the course of the disease.