Movement Disorders in Systemic Diseases

Poewe, Werner; Djamshidian, Atbin

doi:10.1016/j.ncl.2014.09.015

Cited by 13 publications

(13 citation statements)

References 104 publications

(148 reference statements)

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“…Although aging, oxidative damage, and neuroinflammation have been recognized to play crucial roles in the pathogenesis of PD, the precise etiology remains obscure ( van der Brug et al, 2015 ; Volta et al, 2015 ). Emerging evidence suggests PD is a systemic metabolic disease, and metabolic abnormality correlates with functional alternations in PD ( Lu and Hu, 2012 ; Poewe and Djamshidian-Tehrani, 2015 ). Notably, our previous study demonstrated that metabolic inflammation exacerbates DA neuronal degeneration in response to acute 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) challenge in type 2 diabetes mice ( Wang et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Metformin Prevents Dopaminergic Neuron Death in MPTP/P-Induced Mouse Model of Parkinson’s Disease via Autophagy and Mitochondrial ROS Clearance

Qiao

et al. 2016

IJNPPY

198

131

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Background:Our previous study demonstrated that metabolic inflammation exacerbates dopaminergic neuronal degeneration in type 2 diabetes mice. Metformin, a typical oral hypoglycemic agent for diabetes, has been regarded as an activator of AMP-activated protein kinase and a regulator of systemic energy metabolism. Although metformin plays potential protective effects in many disorders, it is unclear whether metformin has a therapeutic role in dopaminergic neuron degeneration in Parkinson’s disease.Methods:In the present study, a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine plus probenecid-induced mouse model of Parkinson’s disease was established to explore the neuroprotective effect of metformin on dopaminergic neurons in substania nigra compacta. We next cultured SH-SY5Y cells to investigate the mechanisms for the neuroprotective effect of metformin.Results:We showed that treatment with metformin (5mg/mL in drinking water) for 5 weeks significantly ameliorated the degeneration of substania nigra compacta dopaminergic neurons, increased striatal dopaminergic levels, and improved motor impairment induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine plus probenecid. We further found that metformin inhibited microglia overactivation-induced neuroinflammation in substania nigra compacta of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine plus probenecid Parkinson’s disease mice, which might contribute to the protective effect of metformin on neurodegeneration. Furthermore, metformin (2mM) activated AMP-activated protein kinase in SH-SY5Y cells, in turn inducing microtubule-associated protein 1 light chain 3-II-mediated autophagy and eliminating mitochondrial reactive oxygen species. Consequently, metformin alleviated MPP+-induced cytotoxicity and attenuated neuronal apoptosis.Conclusions:Our findings demonstrate that metformin may be a pluripotent and promising drug for dopaminergic neuron degeneration, which will give us insight into the potential of metformin in terms of opening up novel therapeutic avenues for Parkinson’s disease.

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Section: Introductionmentioning

confidence: 99%

Metformin Prevents Dopaminergic Neuron Death in MPTP/P-Induced Mouse Model of Parkinson’s Disease via Autophagy and Mitochondrial ROS Clearance

Qiao

et al. 2016

IJNPPY

198

131

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“…It is mainly due to vascular, hereditary, metabolic or drug-induced causes and poses a diagnostic challenge in elderly patients [1] . Polycythemia vera is a sporadic myeloproliferative disorder of the haematopoietic stem cells with an annual incidence of 2–10 cases per million population, and is one of the treatable causes of chorea that must be considered during the diagnostic approach [1–3] .…”

Section: Discussionmentioning

confidence: 99%

“…Neurologic manifestations of polycythemia vera are present in 50–80% of cases, and include headache, vertigo, stroke, visual disturbances and extrapyramidal syndromes, in contrast to chorea which is a rare and infrequently reported complication present in 0.5–5% of patients [3, 4] . This association was first reported by Umney and Bordachzi in 1909 [1] and only a few sporadic cases have since been described in the literature.…”

Section: Discussionmentioning

confidence: 99%

Chorea, Pruritus and Polycythemia: Looking for Clues

Rodriguês

Lopes

Marcolino

et al. 2019

European Journal of Case Reports in Internal Medicine

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Chorea is a movement disorder usually due to vascular, hereditary, metabolic or drug- induced causes, and has rarely been reported in association with polycythemia vera (PV). Polycythemic chorea is an uncommon clinical entity that occurs more often in elderly women. PV is a treatable cause of chorea and must be considered during the diagnostic approach. We report the case of a 75-year-old woman with involuntary movements of the mouth and face with subsequent involvement of the trunk and limbs who was admitted for investigation of the chorea. The patient had the haematological attributes of PV and a positive mutation in the janus kinase 2 (JAK2) gene, and was therefore treated with hydroxyurea which led to a marked reduction in the chorea and improvement in haematological parameters. Various aetiologies of chorea must be considered in the elderly. The present case illustrates the importance of considering PV in the differential diagnosis, since its treatment leads to chorea resolution, thus avoiding serious complications.

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“…Symptoms may improve during sleep or in a supine position. Huntington's disease, Wilson's disease, prion diseases, Sydenham chorea, systemic lupus erythematosus, antiphospholipid antibody syndrome, anti-N-methyl-D-aspartate receptor encephalitis and other autoimmune diseases as illustrated [31][32][33][34][35] in Table 6. The workup may include selected laboratory studies, as well as imaging modalities such as CT, MRI or positron emission tomography (PET).…”

Section: Akathisiamentioning

confidence: 99%

Identification and management of tardive dyskinesia: A case series and literature review

Khouzam

2015

Postgraduate Medicine

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Tardive dyskinesia (TD) is a serious, disabling and potentially permanent, neurological hyperkinetic movement disorder that occurs after months or years of taking dopamine receptor-blocking agents. The pathophysiology of TD is complex, multifactorial and still not fully understood. Although there is no identified effective and standard treatment for TD, several agents have been tried for the management of this motor disturbance. The aim of this case series is to review the literature in regard to the identification, diagnosis and the treatment of TD with anticholinergics, anticholinergic medication withdrawal, cholinergic agents, botulinum toxin intramuscular injections, tetrabenazine, levetiracetam, propranolol and zolpidem, and to describe one case of TD that responded favorably to clonazepam and two cases of TD that responded favorably to Ginkgo biloba.

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Movement Disorders in Systemic Diseases

Cited by 13 publications

References 104 publications

Metformin Prevents Dopaminergic Neuron Death in MPTP/P-Induced Mouse Model of Parkinson’s Disease via Autophagy and Mitochondrial ROS Clearance

Metformin Prevents Dopaminergic Neuron Death in MPTP/P-Induced Mouse Model of Parkinson’s Disease via Autophagy and Mitochondrial ROS Clearance

Chorea, Pruritus and Polycythemia: Looking for Clues

Identification and management of tardive dyskinesia: A case series and literature review

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