Parkinson’s disease

Multiple system atrophy (MSA) is a fatally progressive neurodegenerative disease characterized by variable combinations of parkinsonism, cerebellar ataxia and autonomic dysfunction. The study aimed to describe lower urinary tract symptoms and residual urine volume in early MSA.

7p viormkorn 27-09-2024 4 1   Download

Bài viết mô tả các biến chứng rối loạn vận động và một số yếu tố liên quan ở bệnh nhân mắc bệnh Parkinson được điều trị bằng levodopa. Mô tả cắt ngang 118 bệnh nhân chẩn đoán bệnh Parkinson theo tiêu chuẩn lâm sàng bệnh Parkinson của Hội Rối loạn Vận động (Movement Disorder Society Clinical Diagnostic Criteria for Parkinson’s disease) được điều trị bằng levodopa tại Bệnh viện Bạch Mai và Bệnh viện Đa khoa Hồng Phát, từ tháng 08/2019 đến tháng 06/2020.

5p vinamtan 06-09-2024 1 0   Download

Bài viết mô tả rối loạn dáng đi và thăng bằng ở bệnh nhân Parkinson. Đối tượng và phương pháp nghiên cứu: Mô tả cắt ngang 98 bệnh nhân chẩn đoán bệnh Parkinson theo tiêu chuẩn lâm sàng bệnh Parkinson của Hội Rối loạn Vận động (Movement Disorder Society Clinical Diagnostic Criteria for Parkinson’s disease) điều trị tại bệnh viện Lão khoa Trung ương từ tháng 10 năm 2019 đến tháng 07 năm 2020.

4p vinamtan 06-09-2024 2 0   Download

Bệnh Parkinson (PD: Parkinson’s disease) là bệnh đa yếu tố, có thể do sự tương tác bởi nhiều gen hoặc do sự thay đổi tính nhạy cảm của các alen, các yếu tố môi trường, hoặc do tương tác qua lại giữa môi trường và biểu hiện gen, từ đó làm ảnh hưởng đến hệ thần kinh. Bài viết trình bày xây dựng quy trình phát hiện đột biến gen PARK7 bằng giải trình tự Sanger trên 20 bệnh nhân Parkinson khởi phát sớm.

5p vioraclene 16-04-2024 8 3   Download

The present study will examine the factors that are related to the process and maintenance of resilience and positive functioning in the daily lives of people living with PD compared to those without PD (Kralik et al., 2006; Luthar et al., 2000; Ravenek et al., 2017). In addition, as related to Garroway (2015), the present study will explore the degree to which mediating factors differ between shorter duration, less symptomatically severe groups (early stages) and longer duration, typically more symptomatically severe groups (late stages).

79p runthenight04 02-02-2023 4 2   Download

Regulator of G protein signaling (RGS) proteins are gatekeepers regulating the cellular responses induced by G protein-coupled receptor (GPCR)-mediated activation of heterotrimeric G proteins. Specifically, RGS proteins determine the magnitude and duration of GPCR signaling by acting as a GTPase-activating protein for Gα subunits, an activity facilitated by their semiconserved RGS domain. The R7 subfamily of RGS proteins is distinguished by two unique domains, DEP/DHEX and GGL, which mediate membrane targeting and stability of these proteins.

13p caothientrangnguyen 09-05-2020 24 1   Download

Regulator of G-protein signaling (RGS) proteins were originally identified as negative regulators of G-protein-coupled receptor (GPCR) signaling via their GTPase-accelerating protein (GAP) activity. All RGS proteins contain evolutionarily conserved RGS domain; however, they differ in their size and regulatory domains. RGS1 and RGS10 are smaller than other RGS proteins, and their functions involve various inflammatory responses including autoimmune responses in both the periphery and the central nervous system (CNS). Neuroinflammation is the chronic inflammatory response in the CNS.

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Parkinson’s disease is characterized by the loss of dopaminergic neurons in the nigrostriatal pathway accompanied by the presence of intracellular cytoplasmic inclusions, termed Lewy bodies. Fibrillized a-synuclein forms the major component of Lewy bodies. We reported a specific interaction between rata-synuclein and tat binding protein 1, a subunit of PA700, the regulatory complex of the 26S proteasome.

11p fptmusic 11-04-2013 36 1   Download

Misfolded proteins, aggregates, and inclusion bodies are hall-marks of the cytopathology of neurodegenerative disorders including Huntington’s disease, Amyotropic lateral sclerosis, Parkinson’s disease, Prion diseases, and Alzheimer’s disease. The appearance of proteins with altered folded states is regula-ted by the protein folding quality control machinery and age-dependent. We have identified an unexpected molecular link between metabolic state, accumulation of damaged proteins, the heat-shock response and chaperones, and longevity....

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Neurodegenerative disorders, such as Huntington’s, Alzheimer’s, and Parkinson’s diseases, affect millions of people worldwide and currently there are few effective treatments and no cures for these diseases. Transgenic mice expressing human transgenes for huntingtin, amyloid precursor protein, and other genes associated with familial forms of neurodegenerative disease in humans provide remarkable tools for studying neurodegeneration because they mimic many of the pathological and behavioural features of the human conditions. ...

15p awards 06-04-2013 39 4   Download

A large number of neurodegenerative diseases in humans result from pro-tein misfolding and aggregation. Protein misfolding is believed to be the primary cause of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Creutzfeldt–Jakob disease, cystic fibrosis, Gaucher’s disease and many other degenerative and neurodegenerative disorders.

19p inspiron33 26-03-2013 67 5   Download

a-synuclein is one of a family of proteins whose function remains unknown. This protein has become linked to a number of neurodegenera-tive disease although its potential causative role in these diseases remains mysterious. In diseases such as Parkinson’s disease and Lewy body demen-tias, a-synuclein becomes deposited in aggregates termed Lewy bodies.

9p galaxyss3 21-03-2013 50 3   Download

Accumulation ofa-synuclein resulting in the formation of oligomers and protofibrils has been linked to Parkinson’s disease and Lewy body demen-tia. In contrast, b-synuclein (b-syn), a close homologue, does not aggregate and reducesa-synuclein (a-syn)-related pathology.

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Parkinson’s disease (PD) is a heterogeneous movement disorder character-ized by progressive degeneration of dopamine neurons in substantia nigra. We have previously presented genetic evidence for the possible involvement of alcohol and aldehyde dehydrogenases (ADH; ALDH) by identifying genetic variants in ADH1C and ADH4 that associate with PD.

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N-methyl-norsalsolinol and related tetrahydroisoquinolines accumulate in the nigrostriatal system of the human brain and are increased in the cere-brospinal fluid of patients with Parkinson’s disease. We show here that 6,7-dihydroxylated tetrahydroisoquinolines such asN-methyl-norsalsolinol inhibit tyrosine hydroxylase, the key enzyme in dopamine synthesis, by imitating the mechanisms of catecholamine feedback regulation.

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Parkinson’s disease (PD), a common progressive neurodegenerative disor-der, is characterized by degeneration of dopamine neurons in the substantia nigra and neuronal proteinaceous aggregates called Lewy bodies (LBs). The etiology of PD is probably a combination of environmental and genetic factors.

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L-3,4-Dihydroxyphenylalanine (L-dopa) remains the most effective phar-macological treatment for relief of the severe motor impairments of Par-kinson’s disease. It is very effective in controlling parkinsonian symptoms in the initial phase of the disease, but its action wanes with time. Such ‘wearing-off’ imposes an escalation in the dosage of the drug, which ulti-mately fails to provide stable control of motor symptoms and results in the appearance of abnormal involuntary movements or dyskinesia....

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Protein aggregation can proceed via disordered or ordered mechanisms, with the latter being associated with amyloid fibril formation, which has been linked to a number of debilitating conditions including Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob diseases. Small heat-shock proteins (sHsps), such as aB-crystallin, act as chaperones to prevent protein aggre-gation and are thought to play a key role in the prevention of protein-mis-folding diseases.

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This review explores the possibility that acetylcholinesterase may play a pivotal, non-hydrolytic role in neurodegeneration. More specifically, C-ter-minal sequences of acetylcholinesterase may act as signalling molecules in key brain regions characteristically vulnerable to Alzheimer’s, Parkinson’s and motor neuron disease.

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Heterozygous loss-of-function mutations at the glucosecerebrosidase locus have recently been shown to be a potent risk factor for Lewy body disease. Based on this observation, we have re-evaluated the likelihood that the dif-ferent PARK loci (defined using clinical criteria for disease) may be misleading attempts to find common pathways to pathogenesis.

7p vinaphone15 28-02-2013 49 3   Download