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Inflammation in Neurodegeneration

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 11706

Special Issue Editor


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Guest Editor
School of Medicine, University of Thessaly, Larissa, Greece
Interests: neuodegenerative disorders; neurogenetics; movement disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There is no doubt that pro-inflammatory immune-mediated mechanisms are pivotal to the pathogenicity and progression of neurodegenerative disorders. In this Special Issue, we would like to highlight the binary role of microglia activation in the pathophysiology of neurodegeneration, both neuroprotective and neuromodulatory. Additionally, we would like to show how the expression of several cytokines implicated in neurons’ degeneration could be used as a biomarker for several disorders.

Viral infections have been studied and correlated to neurodegenerative disorders’ progression, usually operating as trigger factors for the inflammatory process. The gut–brain axis and the possible contribution of peripheral bowel inflammation to neuronal death seems to be main contributors of brain neuroinflammation.  

We would also like to discuss therapeutic approaches concerning neurodegeneration and neuroinflammation, which have been studied in experimental and in vitro models and data stemming from epidemiological studies

Prof. Dr. Georgia Xiromerisiou
Guest Editor

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Keywords

  • immune response
  • inflammation
  • neurodegeneration
  • neuroprotection
  • repair

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Published Papers (3 papers)

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Research

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16 pages, 3511 KiB  
Article
Particulate Matter Exacerbates the Death of Dopaminergic Neurons in Parkinson’s Disease through an Inflammatory Response
by Dabin Choi, Gaheon Lee, Kyung Hwa Kim and Hyunsu Bae
Int. J. Mol. Sci. 2022, 23(12), 6487; https://doi.org/10.3390/ijms23126487 - 10 Jun 2022
Cited by 16 | Viewed by 2665
Abstract
Particulate matter (PM), a component of air pollution, has been epidemiologically associated with a variety of diseases. Recent reports reveal that PM has detrimental effects on the brain. In this study, we aimed to investigate the biological effects of ambient particles on the [...] Read more.
Particulate matter (PM), a component of air pollution, has been epidemiologically associated with a variety of diseases. Recent reports reveal that PM has detrimental effects on the brain. In this study, we aimed to investigate the biological effects of ambient particles on the neurodegenerative disease Parkinson’s disease (PD). We exposed mice to coarse particles (PM10: 2.5–10 μm) for short (5 days) and long (8 weeks) durations via intratracheal instillation. Long-term PM10 exposure exacerbated motor impairment and dopaminergic neuron death in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse models. Short-term PM10 exposure resulted in both pulmonary and systemic inflammatory responses in mice. We further investigated the mechanism underlying PM10-induced neurotoxicity in cocultures of lung LA-4 epithelial cells and RAW264.7 macrophages. PM10 treatment elicited a dramatic increase in proinflammatory mediators in LA-4/RAW264.7 coculture. Treating BV2 microglial cells with PM10-treated conditioned medium induced microglial activation. Furthermore, 1-methyl-4-phenylpyridinium (MPP+) treatment caused notable cell death in N2A neurons cocultured with activated BV2 cells in PM10-conditioned medium. Altogether, our results demonstrated that PM10 plays a role in the neurodegeneration associated with PD. Thus, the impact of PM10 on neurodegeneration could be related to detrimental air pollution-induced systemic effects on the brain. Full article
(This article belongs to the Special Issue Inflammation in Neurodegeneration)
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Review

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29 pages, 1272 KiB  
Review
Post-COVID-19 Parkinsonism and Parkinson’s Disease Pathogenesis: The Exosomal Cargo Hypothesis
by Dimitrios S. Mysiris, George D. Vavougios, Eirini Karamichali, Stamatia Papoutsopoulou, Vasileios T. Stavrou, Eirini Papayianni, Stylianos Boutlas, Theodoros Mavridis, Pelagia Foka, Sotirios G. Zarogiannis, Konstantinos Gourgoulianis and Georgia Xiromerisiou
Int. J. Mol. Sci. 2022, 23(17), 9739; https://doi.org/10.3390/ijms23179739 - 28 Aug 2022
Cited by 14 | Viewed by 6279
Abstract
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease after Alzheimer’s disease, globally. Dopaminergic neuron degeneration in substantia nigra pars compacta and aggregation of misfolded alpha-synuclein are the PD hallmarks, accompanied by motor and non-motor symptoms. Several viruses have been linked to [...] Read more.
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease after Alzheimer’s disease, globally. Dopaminergic neuron degeneration in substantia nigra pars compacta and aggregation of misfolded alpha-synuclein are the PD hallmarks, accompanied by motor and non-motor symptoms. Several viruses have been linked to the appearance of a post-infection parkinsonian phenotype. Coronavirus disease 2019 (COVID-19), caused by emerging severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, has evolved from a novel pneumonia to a multifaceted syndrome with multiple clinical manifestations, among which neurological sequalae appear insidious and potentially long-lasting. Exosomes are extracellular nanovesicles bearing a complex cargo of active biomolecules and playing crucial roles in intercellular communication under pathophysiological conditions. Exosomes constitute a reliable route for misfolded protein transmission, contributing to PD pathogenesis and diagnosis. Herein, we summarize recent evidence suggesting that SARS-CoV-2 infection shares numerous clinical manifestations and inflammatory and molecular pathways with PD. We carry on hypothesizing that these similarities may be reflected in exosomal cargo modulated by the virus in correlation with disease severity. Travelling from the periphery to the brain, SARS-CoV-2-related exosomal cargo contains SARS-CoV-2 RNA, viral proteins, inflammatory mediators, and modified host proteins that could operate as promoters of neurodegenerative and neuroinflammatory cascades, potentially leading to a future parkinsonism and PD development. Full article
(This article belongs to the Special Issue Inflammation in Neurodegeneration)
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12 pages, 2647 KiB  
Review
Τhe Greek Variant in APP Gene: The Phenotypic Spectrum of APP Mutations
by Stefania Kalampokini, Despoina Georgouli, Eleni Patrikiou, Antonios Provatas, Varvara Valotassiou, Panagiotis Georgoulias, Cleanthe Spanaki, Georgios M. Hadjigeorgiou and Georgia Xiromerisiou
Int. J. Mol. Sci. 2021, 22(22), 12355; https://doi.org/10.3390/ijms222212355 - 16 Nov 2021
Cited by 2 | Viewed by 2221
Abstract
Mutations in the gene encoding amyloid precursor protein (APP) cause autosomal dominant inherited Alzheimer’s disease (AD). We present a case of a 68-year-old female who presented with epileptic seizures, neuropsychiatric symptoms and progressive memory decline and was found to carry a novel APP [...] Read more.
Mutations in the gene encoding amyloid precursor protein (APP) cause autosomal dominant inherited Alzheimer’s disease (AD). We present a case of a 68-year-old female who presented with epileptic seizures, neuropsychiatric symptoms and progressive memory decline and was found to carry a novel APP variant, c.2062T>G pLeu688Val. A comprehensive literature review of all reported cases of AD due to APP mutations was performed in PubMed and Web of Science databases. We reviewed 98 studies with a total of 385 cases. The mean age of disease onset was 51.3 ± 8.3 (31–80 years). Mutations were most often located in exons 17 (80.8%) and 16 (12.2%). The most common symptoms were dementia, visuospatial symptoms, aphasia, epilepsy and psychiatric symptoms. Mutations in the β-amyloid region, and specifically exon 17, were associated with high pathogenicity and a younger age of disease onset. We describe the second reported APP mutation in the Greek population. APP mutations may act variably on disease expression and their phenotype is heterogeneous. Full article
(This article belongs to the Special Issue Inflammation in Neurodegeneration)
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