Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements

Parkinson’s disease (PD) is one of the most prevalent neurodegenerative aging disorders characterized by motor and non-motor symptoms due to the selective loss of midbrain dopaminergic (DA) neurons. The decreased viability of DA neurons slowly results in the appearance of motor symptoms such as rigi...

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Main Authors: Longping Yao, Jiayu Wu, Sumeyye Koc, Guohui Lu
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-07-01
Series:Frontiers in Cell and Developmental Biology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcell.2021.655819/full
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author Longping Yao
Jiayu Wu
Sumeyye Koc
Guohui Lu
author_facet Longping Yao
Jiayu Wu
Sumeyye Koc
Guohui Lu
author_sort Longping Yao
collection DOAJ
description Parkinson’s disease (PD) is one of the most prevalent neurodegenerative aging disorders characterized by motor and non-motor symptoms due to the selective loss of midbrain dopaminergic (DA) neurons. The decreased viability of DA neurons slowly results in the appearance of motor symptoms such as rigidity, bradykinesia, resting tremor, and postural instability. These symptoms largely depend on DA nigrostriatal denervation. Pharmacological and surgical interventions are the main treatment for improving clinical symptoms, but it has not been possible to cure PD. Furthermore, the cause of neurodegeneration remains unclear. One of the possible neurodegeneration mechanisms is a chronic inflammation of the central nervous system, which is mediated by microglial cells. Impaired or dead DA neurons can directly lead to microglia activation, producing a large number of reactive oxygen species and pro-inflammatory cytokines. These cytotoxic factors contribute to the apoptosis and death of DA neurons, and the pathological process of neuroinflammation aggravates the primary morbid process and exacerbates ongoing neurodegeneration. Therefore, anti-inflammatory treatment exerts a robust neuroprotective effect in a mouse model of PD. Since discovering the first mutation in the α-synuclein gene (SNCA), which can cause disease-causing, PD has involved many genes and loci such as LRRK2, Parkin, SNCA, and PINK1. In this article, we summarize the critical descriptions of the genetic factors involved in PD’s occurrence and development (such as LRRK2, SNCA, Parkin, PINK1, and inflammasome), and these factors play a crucial role in neuroinflammation. Regulation of these signaling pathways and molecular factors related to these genetic factors can vastly improve the neuroinflammation of PD.
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spelling doaj.art-436031fcc3af4745a8be2a86541e87842022-12-21T21:25:18ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-07-01910.3389/fcell.2021.655819655819Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent AdvancementsLongping Yao0Jiayu Wu1Sumeyye Koc2Guohui Lu3Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, ChinaDepartment of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, ChinaDepartment of Neuroscience, Institute of Health Sciences, Ondokuz Mayıs University, Samsun, TurkeyDepartment of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, ChinaParkinson’s disease (PD) is one of the most prevalent neurodegenerative aging disorders characterized by motor and non-motor symptoms due to the selective loss of midbrain dopaminergic (DA) neurons. The decreased viability of DA neurons slowly results in the appearance of motor symptoms such as rigidity, bradykinesia, resting tremor, and postural instability. These symptoms largely depend on DA nigrostriatal denervation. Pharmacological and surgical interventions are the main treatment for improving clinical symptoms, but it has not been possible to cure PD. Furthermore, the cause of neurodegeneration remains unclear. One of the possible neurodegeneration mechanisms is a chronic inflammation of the central nervous system, which is mediated by microglial cells. Impaired or dead DA neurons can directly lead to microglia activation, producing a large number of reactive oxygen species and pro-inflammatory cytokines. These cytotoxic factors contribute to the apoptosis and death of DA neurons, and the pathological process of neuroinflammation aggravates the primary morbid process and exacerbates ongoing neurodegeneration. Therefore, anti-inflammatory treatment exerts a robust neuroprotective effect in a mouse model of PD. Since discovering the first mutation in the α-synuclein gene (SNCA), which can cause disease-causing, PD has involved many genes and loci such as LRRK2, Parkin, SNCA, and PINK1. In this article, we summarize the critical descriptions of the genetic factors involved in PD’s occurrence and development (such as LRRK2, SNCA, Parkin, PINK1, and inflammasome), and these factors play a crucial role in neuroinflammation. Regulation of these signaling pathways and molecular factors related to these genetic factors can vastly improve the neuroinflammation of PD.https://www.frontiersin.org/articles/10.3389/fcell.2021.655819/fullParkinson’s diseasemicrogliageneticsneuroinflamamationdopaminergic neuronsneurotoxins
spellingShingle Longping Yao
Jiayu Wu
Sumeyye Koc
Guohui Lu
Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements
Frontiers in Cell and Developmental Biology
Parkinson’s disease
microglia
genetics
neuroinflamamation
dopaminergic neurons
neurotoxins
title Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements
title_full Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements
title_fullStr Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements
title_full_unstemmed Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements
title_short Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements
title_sort genetic imaging of neuroinflammation in parkinson s disease recent advancements
topic Parkinson’s disease
microglia
genetics
neuroinflamamation
dopaminergic neurons
neurotoxins
url https://www.frontiersin.org/articles/10.3389/fcell.2021.655819/full
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