Academic Journal
Virus-induced brain pathology and the neuroinflammation-inflammation continuum:the neurochemists view
| العنوان: | Virus-induced brain pathology and the neuroinflammation-inflammation continuum:the neurochemists view |
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| المؤلفون: | Sian-Hulsmann, Jeswinder, Riederer, Peter |
| المصدر: | Sian-Hulsmann , J & Riederer , P 2024 , ' Virus-induced brain pathology and the neuroinflammation-inflammation continuum : the neurochemists view ' , Journal of Neural Transmission , vol. 131 , no. 12 , pp. 1429-1453 . https://doi.org/10.1007/s00702-023-02723-5 |
| سنة النشر: | 2024 |
| المجموعة: | University of Southern Denmark: Research Output / Syddansk Universitet |
| مصطلحات موضوعية: | Alzheimer’s disease, Cytotoxicity, Immunology, Inflammation, Microglia and neuroinflammation, Neurodegeneration, Parkinson’s disease, Viruses, Humans, Neuroinflammatory Diseases/pathology, Neurodegenerative Diseases/pathology, Brain/pathology, Animals, Inflammation/pathology |
| الوصف: | 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 ... |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | application/pdf |
| اللغة: | English |
| DOI: | 10.1007/s00702-023-02723-5 |
| الاتاحة: | https://portal.findresearcher.sdu.dk/da/publications/3892b163-346e-486a-a0da-de437e6ef6c3 https://doi.org/10.1007/s00702-023-02723-5 https://findresearcher.sdu.dk/ws/files/279220155/s00702-023-02723-5.pdf |
| Rights: | info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.AF2FAC51 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1007/s00702-023-02723-5 |
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