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Mutations in TMEM230 are not a common cause of Parkinson's disease

and 207 sporadic PD (SPD) patients. The study also included 200 ET patients consisting of 100 familial ET patients and 100 sporadic ET patients. In addition, 400 healthy subjects served as controls (Table 1). We received approval from the Ethics Committee of Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine. Written informed consent from all participants was obtained. Genomic DNA amplification and Sanger sequencing were done to detect the stop codon. DNASTAR Lasergene MegAlign (v7.1.0) and Chromas (v2.33) were used to conduct sequence alignment. We failed to find any variants in the TAG stop codon in all patients and controls. However, our study had some limitations. First, the sample of our study may be not big enough to detect rare mutations, but it should be noted that the frequency of the mutation in Chinese PD patients was 3.1% in Deng’s study. In that case, we should have identified a few carriers. Second, most of our patients were from eastern China, especially Shanghai, which might be regionally different from the participants in Deng’s study, about which we have no information. Third, although we failed to identify mutations in the TAG codon, we did not assess the whole coding region of TMEM230 either; thus, other mutations in this gene may be present. In conclusion, the stop codon mutation is rare in PD and ET patients from China, especially eastern China, based on our study. Still, additional studies are needed to verify the role of TMEM230 mutations in PD or other neurological diseases.