Journal ArticleDOI
Long non-coding RNA-p21 regulates MPP+-induced neuronal injury by targeting miR-625 and derepressing TRPM2 in SH-SY5Y cells.
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TLDR
A new lnc-p21-miR-625-TRPM2 regulatory network that lnc -p21 regulated MPP + -induced neuronal injury by sponging miR- 625 and upregulating TRPM2 in SH-SY5Y cells, which provide a better understanding for the pathogenesis of PD.About:
This article is published in Chemico-Biological Interactions.The article was published on 2019-07-01. It has received 45 citations till now. The article focuses on the topics: SH-SY5Y & Gene knockdown.read more
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Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases
TL;DR: The ncRNAs that have so far been identified in major neurodegenerative disease etiology and the mechanisms that link nc RNAs with disease-specific phenotypes are reviewed, including HTT aggregation in HD, α-synuclein in PD, and Aβ plaques and hyperphosphorylated Tau in AD.
Journal ArticleDOI
Competing Endogenous RNA Networks as Biomarkers in Neurodegenerative Diseases.
Leticia Moreno-García,Tresa López-Royo,Ana C. Calvo,Janne M. Toivonen,Miriam de la Torre,Laura Moreno-Martínez,Nora Molina,Paula Aparicio,Pilar Zaragoza,Raquel Manzano,Rosario Osta +10 more
TL;DR: Although numerous studies have been carried out, further research is needed to validate these complex interactions between RNAs and the alterations in RNA editing that could provide specific ceRNET profiles for neurodegenerative disorders, paving the way to a better understanding of these diseases.
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Epigenetic mechanisms of neurodegenerative diseases and acute brain injury
TL;DR: This review aims to highlight ways in which epigenetics applies to several commonly researched neurodegenerative diseases and forms of acute brain injury as well as shed light on the benefits of epigenetics-based treatments.
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SNHG1 promotes MPP+-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p.
TL;DR: SNHG 1 aggravates MPP+-induced cellular toxicity in SH-SY5Y cells by regulating PTEN/AKT/mTOR signaling via sponging miR-153-3p, indicating the potential of SNHG1 as a promising therapeutic target for PD.
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Long noncoding RNAs in neurodevelopment and Parkinson's disease.
TL;DR: The role of lncRNAs in the process of neurodevelopment, neural differentiation, synaptic function, and pathogenesis of Parkinson's disease (PD) is reviewed to provide the basis for lncRNA‐based disease diagnosis and drug treatment for PD.
References
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Journal ArticleDOI
Mitochondrial dysfunction and oxidative stress in Parkinson's disease and monogenic parkinsonism
TL;DR: Evidence from both sporadic and genetic forms of Parkinson's disease that implicate both mitochondria and oxidative stress as central players in disease pathogenesis are reviewed.
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The History of Parkinson's Disease: Early Clinical Descriptions and Neurological Therapies
TL;DR: Historically important anatomical, biochemical, and physiological studies identified additional pharmacological and neurosurgical targets for Parkinson's disease and allow modern clinicians to offer an array of therapies aimed at improving function in this still incurable disease.
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The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model: a tool to explore the pathogenesis of Parkinson's disease.
Serge Przedborski,Miquel Vila +1 more
TL;DR: Different contributing factors are reviewed, as is the sequence in which it is believed these factors are acting within the cascade of events responsible for the death of dopaminergic neurons in the MPTP model and in PD.
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Serum interleukin (IL-2, IL-10, IL-6, IL-4), TNFα, and INFγ concentrations are elevated in patients with atypical and idiopathic parkinsonism
Bogdan Brodacki,Jacek Staszewski,Beata Toczylowska,Ewa Kozlowska,Nadzieja Drela,Małgorzata Chalimoniuk,Adam Stępień +6 more
TL;DR: The results argue in favor of the involvement of immunological events in the process of neurodegeneration in AP and PD.
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Inflammation and Adaptive Immunity in Parkinson’s Disease
TL;DR: The immune system is designed to protect the host from infection and injury, however, when an adaptive immune response continues unchecked in the brain, the proinflammatory innate microglial response leads to the accumulation of neurotoxins and eventual neurodegeneration.