4.6 Article

Asymmetrical nigral iron accumulation in Parkinson's disease with motor asymmetry: an explorative, longitudinal and test-retest study

期刊

AGING-US
卷 12, 期 18, 页码 18622-18634

出版社

IMPACT JOURNALS LLC
DOI: 10.18632/aging.103870

关键词

Parkinson's disease; quantitative susceptibility mapping; iron; motor asymmetry

资金

  1. 13th Five-year Plan for National Key Research and Development Program of China [2016YFC1306600]
  2. China Postdoctoral Science Foundation [2019M662082]
  3. National Natural Science Foundation of China [81971577, 81571654, 81701647, 81771820]
  4. Natural Science Foundation of Zhejiang Province [LY17H090020]
  5. Projects of Medical and Health Technology Development Program in Zhejiang Province [2015KYB174]
  6. US National Institutes of Health [R01MH096979]

向作者/读者索取更多资源

Parkinson's disease (PD) is commonly characterized by asymmetrical motor impairment. This study aimed to clarify the iron distributions in PD patients with significant motor asymmetry and their longitudinal alterations. This study included 123 PD patients and 121 normal controls. Thirty-eight PD patients were revisited. PD patients with significant motor asymmetry were identified by using an objective criterion. Inter-group, inter-hemisphere and inter-visit differences of regional tissue susceptibility were analyzed. Iron accumulation in dominantly and non-dominantly affected substantia nigra (SN) were observed in PD patients with motor asymmetry compared with normal controls (p < 0.005, Bonferroni corrected). Iron accumulation in the dominantly affected SN was significantly higher than that in the non-dominantly affected SN (p < 0.01, Bonferroni corrected). After follow-up, time effect on the iron content in SN was observed, directing to decrease in PD patients with motor asymmetry without hemispherical difference (p < 0.05). In conclusion, asymmetrical iron accumulation in SN was associated with the motor asymmetry in PD at baseline, while along the disease evolution iron content in SN became longitudinally decreased. All these findings provide new evidence for PD pathogenesis that the abnormal iron metabolism in SN is complicated and not always unidirectional.

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