We evaluate the association of hypertension with PD in an Asian population and performed a meta-analysis on similar studies to address the effect of hypertension on PD risk. A matched case-control study involving 1342 Chinese subjects (671 PD and 671 age and gender-matched controls (with a mean age of 63.9 ± 9.7 and 63.5 ± 9.8 years, and identical proportion of gender distribution) was conducted. Hypertension increases PD risk by 1.9 times [OR 1.86 (1.46–2.38)]. The literature search identified 618 studies initially; however, only three matched case-control studies (all in Caucasians) met the inclusion criteria for meta-analysis. Overall analysis showed that hypertension decreases PD risk by 0.2 times [OR 0.80 (0.66–0.96)]. Hypertension increases PD risk by 1.9 times in our Asian population. However, a meta-analysis comprising of Caucasian populations showed a protective effect of hypertension suggesting that ethnic differences or other genetic or environmental factors may contribute to the divergent observation. Early diagnosis and treatment of hypertension may potentially reduce the risk of PD, at least in our population.
Background Plasma neurofilament light chain (NfL) levels reflect large calibre myelinated axonal loss; and has been proposed as a blood‐based biomarker for neurodegeneration in dementia and parkinsonian disorders. Recent studies have suggested an association between increased plasma NfL levels and worse global cognition in Parkinson’s Disease (PD) patients. However, its relationship with specific cognitive domains remain unclear. This study thus aims to investigate the association between plasma NfL and cognitive domains in early PD. Method Plasma NfL was measured using Quanterix’s Single Molecule Array (Simoa) technology in a total of 197 subjects (175 early PD patients and 22 healthy controls). Cognitive function was assessed using a standard battery of neuropsychological tests. This included the Mini‐Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) as tests of global cognition, as well as two tests for each of five relevant cognitive domains, namely episodic memory, language, working memory, visuospatial, and executive function. Result PD patients had higher plasma NfL levels (mean=16.3 pg/ml, SD=8.59) compared to healthy controls (mean=12.2 pg/ml, SD=4.18) (p=.023). Amongst PD patients, increased NfL levels associated significantly with worse global cognition scores (MMSE: b=‐1.11 p=.009; MoCA: b=‐1.27, p=.026). In particular, higher levels of plasma NfL significantly correlated with poorer episodic memory (b=‐.541, p=.003) and executive function scores (b=‐.427, p=.002). No significant associations were found between plasma NfL and cognitive measures in healthy controls. Conclusion Higher plasma NfL levels were found in PD patients compared to healthy controls and associated significantly with poorer global cognitive function in PD. Interestingly, higher NfL levels correlated with worse episodic memory and executive function. These results implicate plasma NfL’s role as a potential biomarker for cognition in PD. Further studies are required to validate these findings.
Long alpha-synuclein gene (SNCA) promoter (Rep1) allele-carriers are linked to higher risk for Parkinson’s disease (PD) and faster motor progression. Non-motor symptoms including autonomic, neuropsychiatric, and sleep disorders are common in PD. However, the relationship between SNCA Rep1 microsatellite lengths and non-motor symptoms in early PD remains to be elucidated. 171 consecutive early PD patients were recruited from tertiary clinics and genotyped for Rep1. Multivariable regression analyses were performed to examine associations between Rep1 alleles and non-motor outcome scores. Longer Rep1 alleles significantly associated with higher total Non-Motor Symptom Scale (NMSS) scores ( p =.006) and Hospital Anxiety and Depression Scale (HADS) depression subscale scores ( p =.002), after adjusting for covariates and Bonferroni correction. We demonstrated that SNCA Rep1 allele length influences overall non-motor symptom burden and depression in early PD patients. Further functional studies to evaluate the role of Rep1 in non-dopaminergic systems may unravel new therapeutic targets for non-motor symptoms in PD.
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