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Jacobs et al. investigated the association of environmental factors and prodromal features with incident Parkinson's disease (PD) with special reference to the interaction of genetic factors . The authors constructed polygenic risk scores (PRSs) for the risk assessment. Family history of PD, family history of dementia, non-smoking, low alcohol consumption, depression, daytime somnolence, epilepsy and earlier menarche were selected as PD risk factors. The adjusted odds ratio (OR) (95% confidence interval [CI]) of the highest 10% of PRSs for the risk of PD was 3.37 (2.41 to 4.70). I have some concerns about their study.
Regarding risk/protective factors of PD, Daniele et al. conducted a case-control study to performed a simultaneous evaluation of potential factors of PD . Among 31 environmental and lifestyle factors, 9 factors were extracted by multivariate analysis. The adjusted OR (95% CI) of coffee consumption, smoking, physical activity, family history of PD, dyspepsia, exposure to pesticides, metals, and general anesthesia were 0.6 (0.4-0.9), 0.7 (0.6-0.9), 0.8 (0.7-0.9), 3.2 (2.2- 4.8), 1.8 (1.3-2.4), 2.3 (1.3- 4.2), 5.6 (2.3-13.7), 2.8 (1.5-5.4), and 6.1 (2.9-12.7), respectively. Family history of PD and non-smoking were common risk factors, which had also been reported by several prospective studies.
Regarding smoking, Angelopoulou et al. investigated the association between environmental factors and PD subtypes (early-onset, mid-and-late on...
Regarding smoking, Angelopoulou et al. investigated the association between environmental factors and PD subtypes (early-onset, mid-and-late onset, familial and sporadic) . The adjusted OR (95% CI) of smoking for PD overall, mid-and-late onset PD, familial PD, and sporadic PD were 0.48 (0.35-0.67), 0.46 (0.32-0.66), 0.53 (0.34-0.83) and 0.46 (0.32-0.65), respectively. In addition, there was an inverse linear association of PD with pack-years of smoking, except for early-onset PD. Additionally, the adjusted OR (95% CI) of coffee consumption for PD overall, early-onset PD, and familial PD were 0.52 (0.29-0.91), 0.16 (0.05-0.53) and 0.36 (0.17-0.75), respectively. Although the mechanism of the association might be difficult to be confirmed, smokers have a trend of high prevalence of coffee consumption.
Finally, Li et al. evaluated whether the genetic profile might modify PD development and cerebrospinal fluid (CSF) pathological biomarkers by using single nucleotide polymorphisms (SNPs) and PRSs . Some SNPs had significant correlations with PD, and PRSs could predict PD risk and the age at onset. In contrast, the CSF α-synuclein level had no significant correlation with the PRSs in normal subjects. Anyway, further studies are needed to verify PD determinants and gene-environment interactions.
1. Jacobs BM, Belete D, Bestwick J, et al. Parkinson's disease determinants, prediction and gene-environment interactions in the UK Biobank. J Neurol Neurosurg Psychiatry. 2020 Oct;91(10):1046-1054.
2. Daniele B, Roberta P, Andrea F, et al. Risk factors of Parkinson's disease: Simultaneous assessment, interactions and etiological subtypes. Neurology. 2020 Sep 17 doi: 10.1212/WNL.0000000000010813
3. Angelopoulou E, Bozi M, Simitsi AM, et al. The relationship between environmental factors and different Parkinson's disease subtypes in Greece: Data analysis of the Hellenic Biobank of Parkinson's disease. Parkinsonism Relat Disord. 2019 Oct;67:105-112.
4. Li WW, Fan DY, Shen YY, et al. Association of the polygenic risk score with the incidence risk of Parkinson's disease and cerebrospinal fluid α-Synuclein in a Chinese cohort. Neurotox Res. 2019 Oct;36(3):515-522.