Virus-induced brain pathology and the neuroinflammation-inflammation continuum: the neurochemists view: the neurochemists view
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| Název: | Virus-induced brain pathology and the neuroinflammation-inflammation continuum: the neurochemists view: the neurochemists view |
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| Autoři: | Jeswinder Sian-Hulsmann, Peter Riederer |
| Zdroj: | J Neural Transm (Vienna) |
| Informace o vydavateli: | Springer Science and Business Media LLC, 2024. |
| Rok vydání: | 2024 |
| Témata: | Inflammation, 0301 basic medicine, ddc:610, 0303 health sciences, Cytotoxicity, Inflammation/immunology [MeSH], Immunology, Neuroinflammatory Diseases/metabolism [MeSH], Brain/pathology [MeSH], Humans [MeSH], Neurodegenerative Diseases/metabolism [MeSH], Neuroinflammatory Diseases/pathology [MeSH], Neurodegenerative Diseases/pathology [MeSH], Animals [MeSH], Viruses, Brain/immunology [MeSH], Alzheimer's disease, Microglia and neuroinflammation, Neurology and Preclinical Neurological Studies - Original Article, Brain/metabolism [MeSH], Inflammation/pathology [MeSH], Inflammation/metabolism [MeSH], Neuroinflammatory Diseases/immunology [MeSH], Neurodegenerative Diseases/immunology [MeSH], Neurodegeneration, Parkinson's disease, Brain, Neurodegenerative Diseases, 3. Good health, 03 medical and health sciences, Neuroinflammatory Diseases/pathology, Neuroinflammatory Diseases, Humans, Animals, Brain/pathology, Neurodegenerative Diseases/pathology, Inflammation/pathology |
| Popis: | Fascinatingly, an abundance of recent studies has subscribed to the importance of cytotoxic immune mechanisms that appear to increase the risk/trigger for many progressive neurodegenerative disorders, including Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis, and multiple sclerosis. Events associated with the neuroinflammatory cascades, such as ageing, immunologic dysfunction, and eventually disruption of the blood–brain barrier and the “cytokine storm”, appear to be orchestrated mainly through the activation of microglial cells and communication with the neurons. The inflammatory processes prompt cellular protein dyshomeostasis. Parkinson’s and Alzheimer’s disease share a common feature marked by characteristic pathological hallmarks of abnormal neuronal protein accumulation. These Lewy bodies contain misfolded α-synuclein aggregates in PD or in the case of AD, they are Aβ deposits and tau-containing neurofibrillary tangles. Subsequently, these abnormal protein aggregates further elicit neurotoxic processes and events which contribute to the onset of neurodegeneration and to its progression including aggravation of neuroinflammation. However, there is a caveat for exclusively linking neuroinflammation with neurodegeneration, since it’s highly unlikely that immune dysregulation is the only factor that contributes to the manifestation of many of these neurodegenerative disorders. It is unquestionably a complex interaction with other factors such as genetics, age, and environment. This endorses the “multiple hit hypothesis”. Consequently, if the host has a genetic susceptibility coupled to an age-related weakened immune system, this makes them more susceptible to the virus/bacteria-related infection. This may trigger the onset of chronic cytotoxic neuroinflammatory processes leading to protein dyshomeostasis and accumulation, and finally, these events lead to neuronal destruction. Here, we differentiate “neuroinflammation” and “inflammation” with regard to the involvement of the blood–brain barrier, which seems to be intact in the case of neuroinflammation but defect in the case of inflammation. There is a neuroinflammation-inflammation continuum with regard to virus-induced brain affection. Therefore, we propose a staging of this process, which might be further developed by adding blood- and CSF parameters, their stage-dependent composition and stage-dependent severeness grade. If so, this might be suitable to optimise therapeutic strategies to fight brain neuroinflammation in its beginning and avoid inflammation at all. |
| Druh dokumentu: | Article Other literature type |
| Popis souboru: | application/pdf |
| Jazyk: | English |
| ISSN: | 1435-1463 0300-9564 |
| DOI: | 10.1007/s00702-023-02723-5 |
| Přístupová URL adresa: | https://pubmed.ncbi.nlm.nih.gov/38261034 https://portal.findresearcher.sdu.dk/da/publications/3892b163-346e-486a-a0da-de437e6ef6c3 https://doi.org/10.1007/s00702-023-02723-5 https://repository.publisso.de/resource/frl:6523039 https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-393194 https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/39319 https://doi.org/10.1007/s00702-023-02723-5 https://opus.bibliothek.uni-wuerzburg.de/files/39319/00702_2024_Article_2723.pdf |
| Rights: | CC BY |
| Přístupové číslo: | edsair.doi.dedup.....c32673fa938a1e6cdfd7553e39c0c97c |
| Databáze: | OpenAIRE |
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Nájsť tento článok vo Web of Science | Abstrakt: | Fascinatingly, an abundance of recent studies has subscribed to the importance of cytotoxic immune mechanisms that appear to increase the risk/trigger for many progressive neurodegenerative disorders, including Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis, and multiple sclerosis. Events associated with the neuroinflammatory cascades, such as ageing, immunologic dysfunction, and eventually disruption of the blood–brain barrier and the “cytokine storm”, appear to be orchestrated mainly through the activation of microglial cells and communication with the neurons. The inflammatory processes prompt cellular protein dyshomeostasis. Parkinson’s and Alzheimer’s disease share a common feature marked by characteristic pathological hallmarks of abnormal neuronal protein accumulation. These Lewy bodies contain misfolded α-synuclein aggregates in PD or in the case of AD, they are Aβ deposits and tau-containing neurofibrillary tangles. Subsequently, these abnormal protein aggregates further elicit neurotoxic processes and events which contribute to the onset of neurodegeneration and to its progression including aggravation of neuroinflammation. However, there is a caveat for exclusively linking neuroinflammation with neurodegeneration, since it’s highly unlikely that immune dysregulation is the only factor that contributes to the manifestation of many of these neurodegenerative disorders. It is unquestionably a complex interaction with other factors such as genetics, age, and environment. This endorses the “multiple hit hypothesis”. Consequently, if the host has a genetic susceptibility coupled to an age-related weakened immune system, this makes them more susceptible to the virus/bacteria-related infection. This may trigger the onset of chronic cytotoxic neuroinflammatory processes leading to protein dyshomeostasis and accumulation, and finally, these events lead to neuronal destruction. Here, we differentiate “neuroinflammation” and “inflammation” with regard to the involvement of the blood–brain barrier, which seems to be intact in the case of neuroinflammation but defect in the case of inflammation. There is a neuroinflammation-inflammation continuum with regard to virus-induced brain affection. Therefore, we propose a staging of this process, which might be further developed by adding blood- and CSF parameters, their stage-dependent composition and stage-dependent severeness grade. If so, this might be suitable to optimise therapeutic strategies to fight brain neuroinflammation in its beginning and avoid inflammation at all. |
|---|---|
| ISSN: | 14351463 03009564 |
| DOI: | 10.1007/s00702-023-02723-5 |