Parkinson’S Disease
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2021 ◽  
Vol 92 ◽  
pp. 1-6
Tobias Binder ◽  
Markus A. Hobert ◽  
Teresa Pfrommer ◽  
Edyta Leks ◽  
Oliver Granert ◽  

2021 ◽  
Vol 339 ◽  
pp. 232-234
Matthew J. Haney ◽  
Natalia L. Klyachko ◽  
Yuling Zhao ◽  
Richa Gupta ◽  
Evgeniya G. Plotnikova ◽  

2022 ◽  
Vol 72 ◽  
pp. 72-79
Eliana Nachman ◽  
Patrik Verstreken

2021 ◽  
Sebastiaan van Kessel

2021 ◽  
Vol 80 ◽  
pp. 102878
Aline Prieto Silveira-Ciola ◽  
Lucas Simieli ◽  
Natália Madalena Rinaldi ◽  
Fabio Augusto Barbieri

2021 ◽  
Yi-Qing Lv ◽  
Lin Yuan ◽  
Yan Sun ◽  
Hao-Wen Dou ◽  
Ji-Hui Su ◽  

Abstract Background: Growing evidence suggest the association between Parkinson’s disease (PD) and diabetes mellitus (DM). On a cellular level, it was proven that long-term elevated levels of glucose might lead to nigrostriatal degeneration in PD models. However, the underlying mechanism is still unclear. Previously, we have elucidated the potential of type 2 diabetes mellitus (T2DM) in facilitating PD progression, involving aggregation of both alpha-synuclein (α-syn) and islet amyloid polypeptide (IAPP) in the pancreatic and brain tissues. However, due to the complicated effect of insulin resistance on PD onset, the actual mechanism of hyperglycemia-induced dopaminergic degeneration remains unknown. Methods: In the present study, we employed the type 1 diabetes mellitus (T1DM) model induced by streptozotocin (STZ) injection, to investigate the direct effect of elevated blood glucose level on nigrostriatal degeneration. Results: We found that STZ treatment induced more severe pathological alterations in the pancreatic islets and T1DM symptoms in α-syn-overexpression mice than that in wild type (WT) mice, one month and three months after STZ injections. Behavioral tests evaluating motor performance confirmed the nigrostriatal degeneration. Furthermore, we observed a marked decrease in dopaminergic profiles and an increase of α-syn accumulation and Serine 129 (S129) phosphorylation in STZ-treated α-syn mice compared with vehicle-treated mice. At last, we observed more severe neuroinflammation in the brain of the STZ-treated α-syn mice.Conclusion: Our results solidify the potential link between DM and PD, providing insights on how hyperglycemia induces nigrostriatal degeneration and contributes to pathogenetic mechanisms in PD.

Makoto Naoi ◽  
Wakako Maruyama ◽  
Masayo Shamoto-Nagai

2021 ◽  
Vol 0 (0) ◽  
Gege Yu ◽  
Yonghui Wang ◽  
Jinhua Zhao

Abstract Extensive studies have reported that interaction of α-synuclein amyloid species with neurons is a crucial mechanistic characteristic of Parkinson’s disease (PD) and small molecules can downregulate the neurotoxic effects induced by protein aggregation. However, the exact mechanism(s) of these neuroprotective effects by small molecules remain widely unknown. In the present study, α-synuclein samples in the amyloidogenic condition were aged for 120 h with or without different concentrations of mitoquinone (MitoQ) as a quinone derivative compound and the amyloid characteristics and the relevant neurotoxicity were evaluated by Thioflavin T (ThT)/Nile red fluorescence, Congo red absorption, circular dichroism (CD), transmission electron microscopy (TEM), cell viability, lactate dehydrogenase (LDH), reactive oxygen species (ROS), reactive nitrogen species (RNS), malondialdehyde (MDA), superoxide dismutase (SOD), and caspase-9/-3 activity assays. Results clearly showed the capacity of MitoQ on the inhibition of the formation of α-synuclein fibrillation products through modulation of the aggregation pathway by an effect on the kinetic parameters. Also, it was shown that α-synuclein samples aged for 120 h with MitoQ trigger less neurotoxic effects against SH-SY5Y cells than α-synuclein amyloid alone. Indeed, co-incubation of α-synuclein with MitoQ reduced the membrane leakage, oxidative and nitro-oxidative stress, modifications of macromolecules, and apoptosis.

2021 ◽  
Vol 12 ◽  
Shangpei Wang ◽  
Huanhuan Cai ◽  
Zong Cao ◽  
Chuan Li ◽  
Tong Wu ◽  

Background: The thalamus is not only a key relay node of the thalamocortical circuit but also a hub in the regulation of gait. Previous studies of resting-state functional magnetic resonance imaging (fMRI) have shown static functional connectivity (FC) between the thalamus and the cortex are disrupted in Parkinson's disease (PD) patients with freezing of gait (FOG). However, temporal dynamic FC between the thalamus and the cortex has not yet been characterized in these patients.Methods: Fifty PD patients, including 25 PD patients with FOG (PD-FOG) and 25 PD patients without FOG (PD-NFOG), and 25 healthy controls (HC) underwent resting-state fMRI. Seed-voxel-wise static and dynamic FC were calculated between each thalamic nuclei and other voxels across the brain using the 14 thalamic nuclei in both hemispheres as regions of interest. Associations between altered thalamic FC based on significant inter-group differences and severity of FOG symptoms were also examined in PD-FOG.Results: Both PD-FOG and PD-NFOG showed lower static FC between the right lateral posterior thalamic nuclei and right inferior parietal lobule (IPL) compared with HC. Altered FC dynamics between the thalamic nuclei and several cortical areas were identified in PD-FOG, as shown by temporal dynamic FC analyses. Specifically, relative to PD-NFOG or HC, PD-FOG showed greater fluctuations in FC between the left intralaminar (IL) nuclei and right IPL and between the left medial geniculate and left postcentral gyrus. Furthermore, the dynamics of FC between the left pulvinar anterior nuclei and left inferior frontal gyrus were upregulated in both PD-FOG and PD-NFOG. The dynamics of FC between the right ventral lateral nuclei and left paracentral lobule were elevated in PD-NFOG but were maintained in PD-FOG and HC. The quantitative variability of FC between the left IL nuclei and right IPL was positively correlated with the clinical scales scores in PD-FOG.Conclusions: Dynamic FC between the thalamic nuclei and relevant associative cortical areas involved in sensorimotor integration or cognitive function was disrupted in PD-FOG, which was reflected by greater temporal fluctuations. Abnormal dynamic FC between the left IL nuclei of the thalamus and right IPL was related to the severity of FOG.

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Samuel Ånfors ◽  
Ann-Sofi Kammerlind ◽  
Maria H. Nilsson

Abstract Background People with Parkinson’s disease are less physically active than controls. It is important to promote physical activity, which can be assessed using different methods. Subjective measures include physical activity questionnaires, which are easy and cheap to administer in clinical practice. Knowledge of the psychometric properties of physical activity questionnaires for people with Parkinson’s disease is limited. The aim of this study was to evaluate the test-retest reliability of physical activity questionnaires in individuals with Parkinson’s disease without cognitive impairment. Methods Forty-nine individuals with Parkinson’s disease without cognitive impairment participated in a test-retest reliability study. At two outpatient visits 8 days apart, the participants completed comprehensive questionnaires and single-item questions: International Physical Activity Questionnaire-Short Form (IPAQ-SF), Physical Activity Scale for the Elderly (PASE), Saltin-Grimby Physical Activity Level Scale (SGPALS) and Health on Equal Terms (HOET). Test-retest reliability was evaluated using the intraclass correlation coefficient (ICC), standard error of measurement (SEM), limits of agreement, weighted kappa or the Svensson method. Results Several of the physical activity questionnaires had relatively low test-retest reliability, including the comprehensive questionnaires (IPAQ-SF and PASE). Total physical activity according to IPAQ-SF had an ICC value of 0.46 (95% confidence interval [CI], 0.21–0.66) and SEM was 2891 MET-min/week. The PASE total score had an ICC value of 0.66 (95% CI, 0.46–0.79), whereas the SEM was 30 points. The single-item scales of SGPALS-past six months (SGPALS-6 m) and HOET question 1 (HOET-q1) with longer time frames (6 or 12 months, respectively) showed better results. Weighted kappa values were 0.64 (95% CI, 0.45–0.83) for SGPALS-6 m and 0.60 (95% CI, 0.39–0.80) for HOET-q1, whereas the single-item questions with a shorter recall period had kappa values < 0.40. Conclusions Single-item questions with a longer time frame (6 or 12 months) for physical activity were shown to be more reliable than multi-item questionnaires such as the IPAQ-SF and PASE in individuals with Parkinson’s disease without cognitive impairments. There is a need to develop a core outcome set to measure physical activity in people with Parkinson’s disease, and there might be a need to develop new physical activity questionnaires.

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