Vascular risk factors, white matter lesions and cognitive impairment in Parkinson’s disease: the PACOS longitudinal study

Luca, Antonina; Baschi, Roberta; Cicero, Calogero Edoardo; Mostile, Giovanni; Davi, Maria; Bianca, Giuseppe La; Restivo, Vincenzo; Zappia, Mario; Monastero, Roberto

doi:10.1007/s00415-020-10189-8

Cited by 28 publications

(25 citation statements)

References 35 publications

(79 reference statements)

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“…This finding needs further confirmation in larger prospective studies. Several following‐up studies 89,90 revealed that WMH on longitudinal changes may increase the risks for cognitive decline in PD. The greater baseline WMH burden showed, the more significantly cognitive decline in Parkinson's patients, suggesting baseline WMH burden could be the risk for future cognitive decline.…”

Section: Discussionmentioning

confidence: 99%

The influence of white matter hyperintensity on cognitive impairment in Parkinson's disease

Liu

Deng

Xie

et al. 2021

Ann Clin Transl Neurol

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The aim of this meta‐analysis was to review systematically and to identify the relationship between the severity and location of white matter hyperintensities (WMHs) and the degree of cognitive decline in patients with Parkinson’s disease (PD). We searched the PubMed, EMBASE, Web of Science, Ovid, and Cochrane Library databases for clinical trials of the severity and location of WMHs on the degree of cognitive impairment in PD through October 2020. We conducted the survey to compare the association of WMH burden in patients with PD with mild cognitive impairment (PD‐MCI) versus those with normal cognition (PD‐NC) and in patients with PD with dementia (PDD) versus those with PD without dementia (PD‐ND). Nine studies with PD‐MCI versus PD‐NC and 10 studies with PDD versus PD‐ND comparisons were included. The WMH burden in PD‐MCI patients was significantly different compared to that in PD‐NC patients (standard mean difference, SMD = 0.39, 95% CI: 0.12 to 0.66, p = 0.005), while there was no correlation shown in the age‐matched subgroup of the comparison. In addition, PDD patients had a significantly higher burden of WMHs (SMD = 0.8, 95% CI: 0.44 to 1.71, p < 0.0001), especially deep white matter hyperintensities (SMD = 0.54, 95% CI: 0.36 to 0.73, p < 0.00001) and periventricular hyperintensities (SMD = 0.70, 95% CI: 0.36 to 1.04, p < 0.0001), than PD‐NC patients, regardless of the adjustment of age. WMHs might be imaging markers for cognitive impairment in PDD but not in PD‐MCI, regardless of age, vascular risk factors, or race. Further prospective studies are needed to validate the conclusions.

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Section: Discussionmentioning

confidence: 99%

The influence of white matter hyperintensity on cognitive impairment in Parkinson's disease

Liu

Deng

Xie

et al. 2021

Ann Clin Transl Neurol

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“…Parkinson's disease patients frequently suffer from mild cognitive impairment (MCI) (MoCA score more than 21 and less than 26) (Litvan et al, 2012), who are at higher risk of developing dementia compared to PD patients with normal cognition (PD-NC) (Kehagia et al, 2010). Several lines of evidence suggested the inflammatory risk factors (Trefoil Factor 3,neutrophils,lymphocytes,et al) in PD may modulate underlying neurodegeneration particularly in relation to dementia (Stojkovic et al, 2018;Zou et al, 2018;Nicoletti et al, 2020;Wang et al, 2020). It is promising to detect MRI-visible EPVS burden as a marker of cognitive decline in PD.…”

Section: Discussionmentioning

confidence: 99%

Different Perivascular Space Burdens in Idiopathic Rapid Eye Movement Sleep Behavior Disorder and Parkinson’s Disease

Song

et al. 2020

Front. Aging Neurosci.

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Background: Excessive aggregation of α-synuclein is the key pathophysiological feature of Parkinson's disease (PD). Rapid eye movement sleep behavior disorder (RBD) is also associated with synucleinopathies and considered as a powerful predictor of PD. Growing evidence suggests the diminished clearance of α-synuclein may be partly attributable to poor interstitial fluid drainage, which can be reflected by magnetic resonance imaging (MRI)-visible enlarged perivascular space (EPVS). However, the effect of MRI-visible EPVS on iRBD and PD, and their correlation with clinical characteristics remain unclear. Objective: To evaluate the clinical and neuroimaging significance of MRI-visible EPVS in iRBD and PD patients. Methods: We enrolled 33 iRBD patients, 82 PD (with and without RBD) patients, and 35 healthy controls (HCs), who underwent clinical evaluation and 3.0 Tesla MRI. Two neurologists assessed MRI-visible EPVS in centrum semiovale (CSO), basal ganglia (BG), substantia nigra (SN), and brainstem (BS). Independent risk factors for iRBD and PD were investigated using multivariable logistic regression analysis. Spearman analysis was used to test the correlation of MRI-visible EPVS with clinical characteristics of patients. Results: iRBD patients had significantly higher EPVS burdens (CSO, BG, SN, and BS) than PD patients. Higher CSO-EPVS and BS-EPVS burdens were independent risk factors for iRBD. Furthermore, higher CSO-EPVS and SN-EPVS burdens were positively correlated with the severity of clinical symptom in iRBD patients, and higher BG-EPVS burden was positively correlated with the severity of cognitive impairment in PD patients. Conclusion: iRBD and PD patients have different MRI-visible EPVS burdens, which may be related with a compensatory mechanism in glymphatic system. Lower MRI-visible EPVS burden in PD patients may be a manifestation of severe brain waste drainage dysfunction. These findings shed light on the pathophysiologic relationship between iRBD and PD with respect to neuroimaging marker of PD.

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“…We assume that polymorphisms in RAS genes may exert an indirect influence on cognitive decline in PD. Some studies revealed a correlation between white matter hyperintensities (WMH) seen in magnetic resonance imaging with dementia in PD [31][32][33]. Taylor et al [34] analysed polymorphisms in both angiotensin II receptors genes: A1166C (rs5186) in AGTR1 and C3123A (rs2148582) in AGTR2.…”

Section: Discussionmentioning

confidence: 99%

Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease

et al. 2021

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Background Renin-angiotensin system (RAS) influences the central nervous system not only through its peripheral impact—the brain possesses its own local RAS. Studies showed altered RAS components in Parkinson’s disease (PD) and their association with oxidative stress which may be linked to neurodegeneration and dementia. Moreover, the protective functions of RAS blockade antagonists against cognitive decline and dementia have been suggested. This study aimed to examine whether genetic variability in RAS genes correlates with cognitive decline in PD. Methods and results We genotyped single nucleotide polymorphisms (SNPs) in angiotensinogen (AGT: rs699, rs4762), angiotensin II receptors (AGTR1: rs5186 and AGTR2: rs5194, rs1403543) genes, as well as insertion/deletion polymorphism in the angiotensin-converting enzyme (ACE I/D) gene in 256 PD patients, divided into three groups: without cognitive decline, with mild cognitive impairment and with PD dementia. We did not find any significant differences in the frequencies of the analysed polymorphisms in any of the groups. Conclusions Despite no direct correlation between the investigated polymorphisms in RAS genes and cognitive decline in PD, we believe the impact of those genotypes may be indirect, affecting RAS blockade treatment.

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Vascular risk factors, white matter lesions and cognitive impairment in Parkinson’s disease: the PACOS longitudinal study

Cited by 28 publications

References 35 publications

The influence of white matter hyperintensity on cognitive impairment in Parkinson's disease

The influence of white matter hyperintensity on cognitive impairment in Parkinson's disease

Different Perivascular Space Burdens in Idiopathic Rapid Eye Movement Sleep Behavior Disorder and Parkinson’s Disease

Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease

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