Cerebral small vessel disease may worsen motor function, cognition, and mood in Parkinson's disease

2021 ◽  
Vol 83 ◽  
pp. 86-92
Author(s):  
Huimin Chen ◽  
Huijuan Wan ◽  
Meimei Zhang ◽  
Genliang Liu ◽  
Xuemei Wang ◽  
...  
2019 ◽  
Vol 75 (4) ◽  
pp. 696-701
Author(s):  
Caterina Rosano ◽  
Andrea L Metti ◽  
Andrea L Rosso ◽  
Stephanie Studenski ◽  
Nicolaas I Bohnen

Abstract Objective Parkinsonian motor signs are common and disabling in older adults without Parkinson’s disease (PD), but its risk factors are not completely understood. We assessed the influence of striatal dopamine levels, cerebral small vessel disease, and other factors on age-related parkinsonian motor signs in non-PD adults. Methods Striatal dopamine transporter (DAT) binding was quantified via [11C]-CFT positron emission tomography in 87 neurologically intact adults (20–85 years, 57.47% female) with concurrent data on: Unified Parkinson’s Disease Rating Scale motor (UPDRSm), white matter hyperintensities (WMH), and other risk factors (grip strength, vibratory sensitivity, cardio- and cerebro-vascular comorbidities). Sex-adjusted nonparametric models first estimated the associations of age, DAT, WMH, and other factors with UPDRSm; next, interactions of age by DAT, WMH, or other factors were tested. To quantify the influence of DAT, WMH, and other risk factors on the main association of age with UPDRSm, multivariable mediation models with bootstrapped confidence intervals (CI) were used. Results Older age, lower DAT, higher WMH, and worse risk factors significantly predicted worse UPDRSm (sex-adjusted p < .04 for all). DAT, but not WMH or other factors, positively and significantly interacted with age (p = .02). DAT significantly reduced the age-UPDRSm association by 30% (results of fully adjusted mediation model: indirect effect: 0.027; bootstrapped 95% CI: 0.0007, 0.074). Conclusions Striatal dopamine appears to influence to some extent the relationship between age and parkinsonian signs. However, much of the variance of parkinsonian signs appears unexplained. Longitudinal studies to elucidate the multifactorial causes of this common condition of older age are warranted.


2012 ◽  
Vol 27 (12) ◽  
pp. 1506-1512 ◽  
Author(s):  
Raymond S. Schwartz ◽  
Glenda M. Halliday ◽  
Dennis J. Cordato ◽  
Jillian J. Kril

2021 ◽  
Vol 22 (9) ◽  
pp. 4958
Author(s):  
Federico Paolini Paoletti ◽  
Simone Simoni ◽  
Lucilla Parnetti ◽  
Lorenzo Gaetani

Brain small vessel disease (SVD) refers to a variety of structural and functional changes affecting small arteries and micro vessels, and manifesting as white matter changes, microbleeds and lacunar infarcts. Growing evidence indicates that SVD might play a significant role in the neurobiology of central nervous system (CNS) neurodegenerative disorders, namely Alzheimer’s disease (AD) and Parkinson’s disease (PD), and neuroinflammatory diseases, such as multiple sclerosis (MS). These disorders share different pathophysiological pathways and molecular mechanisms (i.e., protein misfolding, derangement of cellular clearance systems, mitochondrial impairment and immune system activation) having neurodegeneration as biological outcome. In these diseases, the actual contribution of SVD to the clinical picture, and its impact on response to pharmacological treatments, is not known yet. Due to the high frequency of SVD in adult-aged patients, it is important to address this issue. In this review, we report preclinical and clinical data on the impact of SVD in AD, PD and MS, with the main aim of clarifying the predictability of SVD on clinical manifestations and treatment response.


2016 ◽  
Vol 31 ◽  
pp. 34-40 ◽  
Author(s):  
Heidi Foo ◽  
Elijah Mak ◽  
Ting Ting Yong ◽  
Ming-Ching Wen ◽  
Russell Jude Chander ◽  
...  

2020 ◽  
Vol 41 (12) ◽  
pp. 3617-3624
Author(s):  
Huimin Chen ◽  
Meimei Zhang ◽  
Gengliang Liu ◽  
Xuemei Wang ◽  
Zhan Wang ◽  
...  

2018 ◽  
Vol 58 ◽  
pp. 70-74 ◽  
Author(s):  
Raymond S. Schwartz ◽  
Glenda M. Halliday ◽  
Derrick Soh ◽  
Dennis J. Cordato ◽  
Jillian J. Kril

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