Nervonic Acid Ameliorates Motor Disorder in Mice with Parkinson’s Disease

2021 ◽  
Vol 15 (3) ◽  
pp. 317-324
Author(s):  
Dandong Hu ◽  
Yujuan Cui ◽  
Ji Zhang
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervonic Acid ◽  
Motor Disorder

scholarly journals Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease

2021 ◽  
Vol 12 (1) ◽  
pp. 237-246
Author(s):  
Dandong Hu ◽  
Yujuan Cui ◽  
Ji Zhang
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Tyrosine Hydroxylase ◽  
Mouse Model ◽  
Nervonic Acid ◽  
Motor Disorder ◽  
Behavioral Deficits ◽  
Liver And Kidney ◽  
The Impact

Abstract Objectives Parkinson’s disease (PD) is a kind of common neurodegenerative disease in the world. Previous studies have proved that nervonic acid (NA), extracted from Xanthoceras sorbifolia Bunge, has the potentials of neuroprotection. However, the effect of NA on the PD remained unknown. This study was designed to investigate the NA’s potential function and relative mechanism on motor disorder. Methods 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used for producing parkinsonism motor disorder on male C57BL/6 mice. Toxicity experiments and behavioral assay were performed to evaluate the effect of NA. Besides, the expression levels of tyrosine hydroxylase and α-synuclein, as well as striatal dopamine (DA), serotonin, and their metabolites were explored through immunoblotting and chromatography after NA treatment in vivo. Results We found that NA could alleviate the MPTP-induced behavioral deficits dose-dependently. Moreover, NA has no toxic effects on the mouse liver and kidney. Of note, we found that NA significantly reduced the impact of MPTP impairment and striatal DA, serotonin, and metabolites were remained unaffected. In addition, tyrosine hydroxylase was upregulated while α-synuclein being downregulated and the oxidative stress was partially repressed evidenced by the upregulation of superoxide dismutase and glutathione activity after NA treatment. Conclusion Our findings unveil NA’s potential for protecting motor system against motor disorder in the PD mouse model without any side effects, indicating NA as an alternative strategy for PD symptom remission.

scholarly journals Neuropsychiatric symptoms in Parkinson's disease: aetiology, diagnosis and treatment

2020 ◽  
Vol 26 (6) ◽  
pp. 333-342 ◽  
Author(s):  
Shoned Jones ◽  
Kelli M. Torsney ◽  
Lily Scourfield ◽  
Katie Berryman ◽  
Emily J. Henderson
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuropsychiatric Symptoms ◽  
Treatment Strategies ◽  
Current Treatment ◽  
Motor Disorder ◽  
Dopamine Dysregulation Syndrome ◽  
Disease Aetiology ◽  
Neuropsychiatric Manifestations ◽  
Assessment Scales

SUMMARYHistorically, Parkinson's disease was viewed as a motor disorder and it is only in recent years that the spectrum of non-motor disorders associated with the condition has been fully recognised. There is a broad scope of neuropsychiatric manifestations, including depression, anxiety, apathy, psychosis and cognitive impairment. Patients are more predisposed to delirium, and Parkinson's disease treatments give rise to specific syndromes, including impulse control disorders, dopamine agonist withdrawal syndrome and dopamine dysregulation syndrome. This article gives a broad overview of the spectrum of these conditions, describes the association with severity of Parkinson's disease and the degree to which dopaminergic degeneration and/or treatment influence symptoms. We highlight useful assessment scales that inform diagnosis and current treatment strategies to ameliorate these troublesome symptoms, which frequently negatively affect quality of life.

Stereopsis Deficits in Parkinson’s Disease and Their Clinical Implications

2020 ◽  
Author(s):  
Fang Ba ◽  
Tina T. Sang ◽  
Jaleh Fatehi ◽  
Wenjing He ◽  
Emanuel Mostofi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Disease Severity ◽  
Rating Scale ◽  
Disease Status ◽  
Cognitive Status ◽  
Control Group ◽  
Motor Disorder ◽  
Healthy Control ◽  
Stereo Acuity

Abstract Background: Parkinson's disease (PD) is not exclusively a motor disorder. Among non-motor features, PD patients possess sensory visual dysfunctions. Stereopsis deficit can significantly impact patients' motor performance. However, it is not routinely tested, and its significance is under-investigated. Studying stereopsis using reliable 3D stimuli may help determine its implications in disease status in PD.The objective of the study is to investigate stereopsis abnormalities in PD with reliable and more physiological tools, and their correlation with indicators of PD severity. Methods: Twenty-four healthy control and 20 PD participants were first evaluated for visual acuity, visual field, contrast acuity, and stereoperception with 2D and Titmus stereotests, followed by the assessment with the 3D active shutter system. The correlation between stereopsis and disease severity, Unified Parkinson’s disease rating scale motor scores (UPDRS-III), levodopa equivalent daily dose (LEDD), course of disease and cognitive status were evaluated using univariate regression models. Results: Screening visual tests did not reveal any differences between PD and control group. With the 3D active shutter system, PD patients demonstrated significantly worse stereopsis (i.e p=0.002, 26 seconds of arc). There was a trend that UPDRS-III and LEDD negatively correlate with the stereo acuity, suggesting poorer stereoperception is related to disease severity. Preserved cognitive function correlated with more intact stereo acuity. Conclusion: With more reliable and physiological tools, PD patients exhibit poorer stereopsis. These deficits reflected PD motor and cognitive status. How stereopsis relates to gait, fall risks and navigation warrants more investigations in the future.

scholarly journals FREQUENCY AND CORRELATES OF POOR SLEEP QUALITY AMONG PATIENTS OF PARKINSON’S DISEASE

2020 ◽  
Vol 70 (6) ◽  
pp. 1640-44
Author(s):  
Syed Sakhawat Kazmi ◽  
Zahid Hassan ◽  
Waseem Alamgir ◽  
Asif Hashmat ◽  
Muhammad Ali Yousaf ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Sleep Quality ◽  
Quality Index ◽  
Pittsburgh Sleep Quality Index ◽  
Military Hospital ◽  
Poor Sleep ◽  
Motor Disorder ◽  
Poor Sleep Quality ◽  
Duration Of Illness

Objective: To determine the frequency of poor sleep quality among the patients of Parkinson’s disease (PD) and analyze its relationship with the socio-demographic factors.Study Design: Correlational study. Place and Duration of Study: Pak Emirates Military Hospital Rawalpindi, from Jan 2019 to Jun 2019. Methodology: One hundred and fifty patients of Parkinson’s disease were approached to participate in this study. Pittsburgh sleep quality index (PSQI) was the psychometric tool used to assess the study parameter for the patients. Age, gender, duration of illness, poly pharmacy and tobacco smoking were corelated with presence of poor quality of sleep among the patients of Parkinson’s disease. Results: Out of 150 patients of Parkinson’s disease screened through Pittsburgh sleep quality index, 85 (56.7%)showed the presence of poor sleep quality while 65 (43.3%) had good sleep quality. Mean age of the patients was 66.2 ± 4.648 years. After applying the logistic regression, we found that increasing age and longer duration of illness had significant association with the presence of poor sleep quality among the patients of Parkinson disease. Conclusion: Previously considered a pure motor disorder, Parkinsonism has a lot of other neuro-psychiatricmanifestations as well. Poor sleep quality turned out to be one of these non-motor problems associated with this chronic debilitating illness. Increasing age and longer duration of illness among these patients emerged asindependent risk factors for poor sleep quality in Parkinsonism.

scholarly journals 5-HT2AReceptor Binding in the Frontal Cortex of Parkinson’s Disease Patients and Alpha-Synuclein Overexpressing Mice: A Postmortem Study

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Nadja Bredo Rasmussen ◽  
Mikkel Vestergaard Olesen ◽  
Tomasz Brudek ◽  
Per Plenge ◽  
Anders Bue Klein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Executive Function ◽  
Transgenic Mice ◽  
Frontal Cortex ◽  
Receptor Binding ◽  
Alpha Synuclein ◽  
Association Cortex ◽  
Motor Disorder

The5-HT2Areceptor is highly involved in aspects of cognition and executive function and seen to be affected in neurodegenerative diseases like Alzheimer’s disease and related to the disease pathology. Even though Parkinson’s disease (PD) is primarily a motor disorder, reports of impaired executive function are also steadily being associated with this disease. Not much is known about the pathophysiology behind this. The aim of this study was thereby twofold: (1) to investigate5-HT2Areceptor binding levels in Parkinson’s brains and (2) to investigate whether PD associated pathology, alpha-synuclein (AS) overexpression, could be associated with5-HT2Aalterations. Binding density for the5-HT2A-specific radioligand [3H]-MDL 100.907 was measured in membrane suspensions of frontal cortex tissue from PD patients. Protein levels of AS were further measured using western blotting. Results showed higher AS levels accompanied by increased5-HT2Areceptor binding in PD brains. In a separate study, we looked for changes in5-HT2Areceptors in the prefrontal cortex in 52-week-old transgenic mice overexpressing human AS. We performed region-specific5-HT2Areceptor binding measurements followed by gene expression analysis. The transgenic mice showed lower5-HT2Abinding in the frontal association cortex that was not accompanied by changes in gene expression levels. This study is one of the first to look at differences in serotonin receptor levels in PD and in relation to AS overexpression.

What Genetics Tells us About the Causes and Mechanisms of Parkinson's Disease

2011 ◽  
Vol 91 (4) ◽  
pp. 1161-1218 ◽  
Author(s):  
Olga Corti ◽  
Suzanne Lesage ◽  
Alexis Brice
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Late Onset ◽  
Association Studies ◽  
Lewy Bodies ◽  
Mendelian Inheritance ◽  
Model Systems ◽  
Motor Disorder ◽  
Genome Wide Association Studies ◽  
New Genes

Parkinson's disease (PD) is a common motor disorder of mysterious etiology. It is due to the progressive degeneration of the dopaminergic neurons of the substantia nigra and is accompanied by the appearance of intraneuronal inclusions enriched in α-synuclein, the Lewy bodies. It is becoming increasingly clear that genetic factors contribute to its complex pathogenesis. Over the past decade, the genetic basis of rare PD forms with Mendelian inheritance, representing no more than 10% of the cases, has been investigated. More than 16 loci and 11 associated genes have been identified so far; genome-wide association studies have provided convincing evidence that polymorphic variants in these genes contribute to sporadic PD. The knowledge acquired of the functions of their protein products has revealed pathways of neurodegeneration that may be shared between inherited and sporadic PD. An impressive set of data in different model systems strongly suggest that mitochondrial dysfunction plays a central role in clinically similar, early-onset autosomal recessive PD forms caused by parkin and PINK1, and possibly DJ-1 gene mutations. In contrast, α-synuclein accumulation in Lewy bodies defines a spectrum of disorders ranging from typical late-onset PD to PD dementia and including sporadic and autosomal dominant PD forms due to mutations in SCNA and LRRK2. However, the pathological role of Lewy bodies remains uncertain, as they may or may not be present in PD forms with one and the same LRRK2 mutation. Impairment of autophagy-based protein/organelle degradation pathways is emerging as a possible unifying but still fragile pathogenic scenario in PD. Strengthening these discoveries and finding other convergence points by identifying new genes responsible for Mendelian forms of PD and exploring their functions and relationships are the main challenges of the next decade. It is also the way to follow to open new promising avenues of neuroprotective treatment for this devastating disorder.

scholarly journals Non-motor signs in Parkinson’s disease: a review

2015 ◽  
Vol 73 (5) ◽  
pp. 454-462 ◽  
Author(s):  
Renato P. Munhoz ◽  
Adriana Moro ◽  
Laura Silveira-Moriyama ◽  
Helio A. Teive
Keyword(s):  
Quality Of Life ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Current Knowledge ◽  
Early Recognition ◽  
The Other ◽  
Motor Disorder ◽  
The Past ◽  
Sensory Disturbances

During the past decade the view of Parkinson’s disease (PD) as a motor disorder has changed significantly and currently it is recognized as a multisystem process with diverse non-motor signs (NMS). In addition to been extremely common, these NMS play a major role in undermining functionality and quality of life. On the other hand, NMS are under recognized by physicians and neglected by patients. Here, we review the most common NMS in PD, including cognitive, psychiatric, sleep, metabolic, and sensory disturbances, discuss the current knowledge from biological, epidemiological, clinical, and prognostic standpoints, highlighting the need for early recognition and management.

Stimulation of electron transport as potential novel therapy in Parkinson's disease with mitochondrial dysfunction

2015 ◽  
Vol 43 (2) ◽  
pp. 275-279 ◽  
Author(s):  
Melissa Vos ◽  
Patrik Verstreken ◽  
Christine Klein
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Electron Transport ◽  
Mitochondrial Dysfunction ◽  
Dopaminergic Neurons ◽  
Current Therapy ◽  
Motor Disorder ◽  
Novel Therapy ◽  
Transport Chain ◽  
Stimulation Of

Parkinson's disease (PD) is a neurodegenerative motor disorder characterized by the loss of dopaminergic neurons. This loss of dopaminergic neurons is the pathological hallmark of the disease that results in the characteristic motor syndrome. Restoration of dopamine levels is the basis of current therapy; however, this does not tackle the cause of the disease. While the aetiology of PD remains mostly elusive, mitochondrial dysfunction has been linked to (at least) part of the PD cases. In this review we discuss recent findings in Drosophila melanogaster showing that stimulation of the electron transport chain is beneficial for PD fly models showing Complex I defects and discuss the possible clinical applications of these findings.

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