Non-Motor Symptoms of Parkinson’s Disease and Their Impact on Quality of Life in a Cohort of Moroccan Patients

Tibar, Houyam; Bayad, Khalil El; Bouhouche, Ahmed; Haddou, El Hachmia Ait Ben; Benomar, Ali; Yahyaoui, M.; Benazzouz, Abdelhamid; Regragui, W.

doi:10.3389/fneur.2018.00170

Cited by 90 publications

(71 citation statements)

References 81 publications

(90 reference statements)

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“…Autonomic dysfunction is a core clinical feature underlying all of the α‐synucleinopathies and includes bladder dysfunction, constipation, cardiovascular abnormalities, sexual dysfunction, sialorrhea, dry eyes, excessive sweating, and altered thermoregulation. These symptoms are a greater contributor to loss of quality of life than are the motor symptoms in PD (Estrada‐Bellmann et al, ; Martinez‐Martin, Rodriguez‐Blazquez, Kurtis, Chaudhuri,, & NMSS Validation Group, ; Müller et al, ; Prakash et al, ; Tibar et al, ), yet have been challenging to investigate in model organisms. Although common to all of the α‐synucleinopathies, autonomic dysfunction is particularly important in MSA (Fanciulli & Wenning, ), where it is required to make the diagnosis (Gilman et al, ).…”

Section: Discussionmentioning

confidence: 99%

Glial α‐synuclein promotes neurodegeneration characterized by a distinct transcriptional program in vivo

Olsen

Feany

2019

Glia

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α‐Synucleinopathies are neurodegenerative diseases that are characterized pathologically by α‐synuclein inclusions in neurons and glia. The pathologic contribution of glial α‐synuclein in these diseases is not well understood. Glial α‐synuclein may be of particular importance in multiple system atrophy (MSA), which is defined pathologically by glial cytoplasmic α‐synuclein inclusions. We have previously described Drosophila models of neuronal α‐synucleinopathy, which recapitulate key features of the human disorders. We have now expanded our model to express human α‐synuclein in glia. We demonstrate that expression of α‐synuclein in glia alone results in α‐synuclein aggregation, death of dopaminergic neurons, impaired locomotor function, and autonomic dysfunction. Furthermore, co‐expression of α‐synuclein in both neurons and glia worsens these phenotypes as compared to expression of α‐synuclein in neurons alone. We identify unique transcriptomic signatures induced by glial as opposed to neuronal α‐synuclein. These results suggest that glial α‐synuclein may contribute to the burden of pathology in the α‐synucleinopathies through a cell type‐specific transcriptional program. This new Drosophila model system enables further mechanistic studies dissecting the contribution of glial and neuronal α‐synuclein in vivo, potentially shedding light on mechanisms of disease that are especially relevant in MSA but also the α‐synucleinopathies more broadly.

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Section: Discussionmentioning

confidence: 99%

Glial α‐synuclein promotes neurodegeneration characterized by a distinct transcriptional program in vivo

Olsen

Feany

2019

Glia

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“…For example, PD patients carrying PARKIN , PINK1, or LRRK2 mutation does not always present Lewy bodies [ 216 , 217 ]. Moreover, patients differ in the age of onset, ailment severity, neurodegeneration progression, and symptoms (including motor and non-motor) [ 218 , 219 ].…”

Section: Neurotoxin-induced Experimental In Vivo Models Of Pdmentioning

confidence: 99%

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Prasad

Hung

2020

Antioxidants

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Currently, neurodegenerative diseases are a major cause of disability around the world. Parkinson’s disease (PD) is the second-leading cause of neurodegenerative disorder after Alzheimer’s disease. In PD, continuous loss of dopaminergic neurons in the substantia nigra causes dopamine depletion in the striatum, promotes the primary motor symptoms of resting tremor, bradykinesia, muscle rigidity, and postural instability. The risk factors of PD comprise environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular injury, aging, and hereditary defects. The pathologic features of PD include impaired protein homeostasis, mitochondrial dysfunction, nitric oxide, and neuroinflammation, but the interaction of these factors contributing to PD is not fully understood. In neurotoxin-induced PD models, neurotoxins, for instance, 6-hydroxydopamine (6-OHDA), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-Methyl-4-phenylpyridinium (MPP+), paraquat, rotenone, and permethrin mainly impair the mitochondrial respiratory chain, activate microglia, and generate reactive oxygen species to induce autooxidation and dopaminergic neuronal apoptosis. Since no current treatment can cure PD, using a suitable PD animal model to evaluate PD motor symptoms’ treatment efficacy and identify therapeutic targets and drugs are still needed. Hence, the present review focuses on the latest scientific developments in different neurotoxin-induced PD animal models with their mechanisms of pathogenesis and evaluation methods of PD motor symptoms.

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“…Understanding the inner working mechanisms of PD is one of the most intriguing scientific questions. Studies in neuroscience strongly suggest intervention during early therapeutic windows (Vu et al, 2012;Tibar et al, 2018). Although positron emitted topography/computed tomography is accurate (Meles et al, 2017) the diagnosis of PD at present is mainly dependent on clinical features and scores.…”

Section: Introductionmentioning

confidence: 99%

A Radiomics Approach to Predicting Parkinson’s Disease by Incorporating Whole-Brain Functional Activity and Gray Matter Structure

et al. 2020

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Parkinson's disease (PD) is a progressive, chronic, and neurodegenerative disorder that is primarily diagnosed by clinical examinations and magnetic resonance imaging (MRI). In this study, we proposed a machine learning based radiomics method to predict PD. Fifty healthy controls (HC) along with 70 PD patients underwent restingstate magnetic resonance imaging (rs-fMRI). For all subjects, we extracted five types of 6664 features, including mean amplitude of low-frequency fluctuation (mALFF), mean regional homogeneity (mReHo), resting-state functional connectivity (RSFC), voxelmirrored homotopic connectivity (VMHC) and gray matter (GM) volume. After conducting dimension reduction utilizing Least absolute shrinkage and selection operator (LASSO), fifty-three radiomic features including 46 RSFCs, 1 mALFF, 3 mReHos, 1 VMHC, 2 GM volumes and 1 clinical factor were retained. The selected features also indicated the most discriminative regions for PD. We further conducted model fitting procedure for classifying subjects in the training set employing random forest and support volume machine (SVM) to evaluate the performance of the two methods. After cross-validation, both methods achieved 100% accuracy and area under curve (AUC) for distinguishing between PD and HC in the training set. In the testing set, SVM performed better than random forest with the accuracy, true positive rate (TPR) and AUC being 85%, 1 and 0.97, respectively. These findings demonstrate the radiomics technique has the potential to support radiological diagnosis and to achieve high classification accuracy for clinical diagnostic systems for patients with PD.

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Non-Motor Symptoms of Parkinson’s Disease and Their Impact on Quality of Life in a Cohort of Moroccan Patients

Cited by 90 publications

References 81 publications

Glial α‐synuclein promotes neurodegeneration characterized by a distinct transcriptional program in vivo

Glial α‐synuclein promotes neurodegeneration characterized by a distinct transcriptional program in vivo

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

A Radiomics Approach to Predicting Parkinson’s Disease by Incorporating Whole-Brain Functional Activity and Gray Matter Structure

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