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Regulation and targeting of enzymes mediating Parkinson's disease pathogenesis: focus on Parkinson's disease Kinases, GTPases and ATPases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193998 Year: Pages: 163 DOI: 10.3389/978-2-88919-399-8 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2015-12-10 11:59:06
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Understanding the molecular pathogenesis of Parkinson’s disease (PD) is a priority in biomedical research and a pre-requisite to improve early disease diagnosis and ultimately to developing disease-modifying strategies. In the past decade and a half, geneticists have identified several genes that are involved in the molecular pathogenesis of PD. They not only identified gene variants segregating with familial forms of PD but also genetic risk factors of sporadic PD via genome-wide association studies (GWAS). Understanding how PD genes and their gene products function holds the promise of unraveling key PD pathogenic processes. Therefore the precise cellular role of PD proteins is currently the subject of intense investigation.Interestingly, a number of PD proteins have enzymatic functions, including kinase, GTPase or ATPase functions. In the context of understanding disease pathogenesis or developing disease-modifying therapies, enzymes possess several useful features. Firstly, enzymes are often key elements of cellular signaling networks, acting as on-off switches to determine signaling intensity. For instance, kinases mediate phosphorylation events, which activate or inactivate their substrates, while GTPases modulate activity of their effector proteins via direct interaction in a GDP/GTP dependent manner. ATPases also control cellular processes through their involvement in cellular energy production and/or in transmembrane transport. Secondly, enzymes are attractive targets for therapeutics development. This is exemplified by the growing number of kinase inhibitors approved for clinical use, while compounds modulating GTPases or ATPases have also been proposed as potential therapeutics. Finally, as elements in cellular signaling networks, enzymes are not generally constitutively active but subject to further regulation through additional signaling components. Knowledge of how PD kinases, GTPases and ATPases are activated or inactivated can aid in understanding how PD signaling networks are deregulated in disease and point to new possibilities in targeting pathological signaling processes. The objective of this research topic is to provide an overview of current knowledge on the regulation of cellular signaling networks of PD kinases, GTPases and ATPases. Both upstream and downstream signaling events will be covered, with a focus on molecular events that can readily be monitored (relevance as disease biomarkers) and have a potential to be modulated (relevance as potential therapeutic target).

Parkinson's Disease Cell Vulnerability and Disease Progression

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196760 Year: Pages: 194 DOI: 10.3389/978-2-88919-676-0 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Parkinson's disease is a neurodegenerative disorder that affects 1.5% of the global population over 65 years of age. The hallmark feature of this disease is the degeneration of dopamine neurons in the substantia nigra pars compacta and a consequent striatal dopamine deficiency. The pathogenesis of Parkinson's Disease remains unclear. Despite tremendous growth in recent years in our knowledge of the molecular basis of Parkinson's Disease and the molecular pathways of cell death important questions remain regarding why are substantia nigra cells especially vulnerable, which mechanisms underlie progressive cell loss or what do Lewy bodies or alpha-synuclein reveal about disease progression. Understanding the different vulnerability of the dopaminergic neurons from midbrain regions and the mechanisms whereby pathology becomes widespread are primary objectives of basic and clinical research in Parkinson's Disease.This e-Book discusses the etiopathogenesis of Parkinson's Disease, presenting a series of papers that provide up-to-date, state-of-the-art information on molecular and cellular mechanisms involved in the neurodegeneration process in the disease, the role of activation of functional anatomical organization of the basal ganglia and in particular habitual vs goal directed systems as a factor of neuronal vulnerability, the possibility that Parkinson's Disease coulb be a prion disease and how genetic factors linked to familial and sporadic forms of PD. We hope that this e-Book will stimulate the continuing efforts to understand the cell and physiological mechanisms underlying the origin of Parkinson's Disease.

The Molecular and Cellular Basis for Parkinson's Disease

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ISBN: 9783039215485 9783039215492 Year: Pages: 230 DOI: 10.3390/books978-3-03921-549-2 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Neurology
Added to DOAB on : 2019-12-09 11:49:15
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The focus on dopamine-sensitive motor symptoms, in association with the improvement of motor complications in the heterogeneous disease entity Parkinson's disease, has led to a certain standstill in research. This Special Issue provides new concepts and new ideas on the pathogenesis, genetics, and clinical maintenance of Parkinson's disease and related disorders. Not only new experimental findings, but also clinical outcomes, case series, and research on alternative, non-pharmacological therapies are included. The objective is to bridge the currently increasing gap between experimental and clinical research on Parkinson's disease and related disorders.

Keywords

epigenetics --- Parkinson’s disease --- brain --- DNA methylation --- Parkinson’s disease --- fatty acid ?-oxidation --- long-chain acylcarnitine --- Parkinson’s disease --- fatty acyls --- glycerolipids --- glycerophospholipids --- sphingolipids --- sterol lipids --- lipoproteins --- ?-synuclein-mediated pathology --- disease-modifying effects --- neuroprotection --- autophagy --- cysteinyl-dopamine --- hypochlorite --- oxidative stress --- Parkinson’s disease --- redox cycling --- Parkinson’s disease --- brain iron --- motor dysfunction --- neurometabolites --- magnetic resonance imaging --- magnetic resonance spectroscopy --- GABA --- spectroscopy --- Parkinson’s disease --- neuroinflammation --- alpha-Synuclein --- immunotherapy --- mesenchymal stem cells --- secretome --- exosomes --- Parkinson’s disease --- microRNAs --- Parkinson disease --- multiprofessional therapy --- inpatient treatment --- multimodal complex treatment --- caffeic acid --- chlorogenic acid --- rotenone --- Parkinson’s disease --- neuroprotection --- dopaminergic neuron --- myenteric plexus --- enteric glial cell --- metallothionein --- Parkinson’s disease --- microbiota --- molecular mimicry --- microbiome --- alpha-synuclein --- curli --- gut-brain axis --- neurodegeneration --- glucocerebrosidase --- Parkinson’s disease --- Gaucher’s disease --- Lewy Body Dementia --- REM sleep behavior disorders --- [123I]FP-CIT-SPECT --- DAT --- nigral cells --- Parkinson’s disease --- parkinsonisms --- cell line --- differentiation --- HOG --- immature oligodendrocyte --- Krabbe’s disease --- oligodendrocyte --- mature oligodendrocyte --- MO3.13 --- myelin --- multiple sclerosis --- schizophrenia --- SH-SY5Y

Metabolomics in Neurodegenerative Disease

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ISBN: 9783039280407 / 9783039280414 Year: Pages: 184 DOI: 10.3390/books978-3-03928-041-4 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2020-06-09 16:38:57
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The range of human neurodegenerative diseases continues to pose significant unmet medical needs for societies around the world. The progressive and terminal nature of these conditions places a considerable personal burden on the individual affected but also on public health systems and health services. Tens of millions of people are indiscriminately affected by various dementias, which are rising at an alarming rate. There are no cures for many conditions, and it is clear that treatments applied as early as possible could greatly improve outcomes for patients. Therefore, new disease classification and diagnostic tools should be a key priority. Metabolomics represents a relatively new field of analytical science, which can be extremely useful in the early diagnosis of disease. The relatively unique feature of metabolites is that they sit at the intersection between the genetic background of an organism and its environment. Because many neurodegenerative diseases are not genetically inherited (instead having a range of known genetic risk factors and also a large number of unknown environmental triggers) the field of metabolomics offers great promise for the discovery of new, biologically, and clinically relevant biomarkers for neurodegenerative disorders. It is already bringing forward new knowledge in terms of the mechanisms of neurodegenerative disease.

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