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Events associated with the neuroinflammatory cascades, such as ageing, immunologic dysfunction, and eventually disruption of the blood\u2013brain barrier and the \u201ccytokine storm\u201d, appear to be orchestrated mainly through the activation of microglial cells and communication with the neurons. The inflammatory processes prompt cellular protein dyshomeostasis. Parkinson\u2019s and Alzheimer\u2019s disease share a common feature marked by characteristic pathological hallmarks of abnormal neuronal protein accumulation. These Lewy bodies contain misfolded \u03b1-synuclein aggregates in PD or in the case of AD, they are A\u03b2 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\u2019s 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 \u201cmultiple hit hypothesis\u201d. Consequently, if the host has a genetic susceptibility coupled to an age-related weakened immune system, this\u00a0makes 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 \u201cneuroinflammation\u201d and \u201cinflammation\u201d with regard to the involvement of the blood\u2013brain 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.<\/jats:p>","DOI":"10.1007\/s00702-023-02723-5","type":"journal-article","created":{"date-parts":[[2024,1,23]],"date-time":"2024-01-23T07:01:36Z","timestamp":1705993296000},"page":"1429-1453","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Virus-induced brain pathology and the neuroinflammation-inflammation continuum: the neurochemists view"],"prefix":"10.1007","volume":"131","author":[{"given":"Jeswinder","family":"Sian-Hulsmann","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3453-6335","authenticated-orcid":false,"given":"Peter","family":"Riederer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,1,23]]},"reference":[{"issue":"6116","key":"2723_CR1","doi-asserted-by":"publisher","first-page":"156","DOI":"10.1126\/science.1227901.PMID:23307732;PMCID:PMC4431634","volume":"339","author":"A Aguzzi","year":"2013","unstructured":"Aguzzi A, Barres BA, Bennett ML (2013) Microglia: scapegoat, saboteur, or something else? 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