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Cited by 291

The DOI matches its Crossref record; 78 of the 78 references it cites were found in a registry or an index.

Neuronal injury in bacterial meningitis: mechanisms and implications for therapy

Open access
Nau, Roland, Brück, Wolfgang·2002·Trends in Neurosciences

Abstract

In bacterial meningitis, long-term neurological sequelae and death are caused jointly by several factors: (1) the systemic inflammatory response of the host, leading to leukocyte extravasation into the subarachnoid space, vasculitis, brain edema and secondary ischemia; (2) stimulation of resident microglia within the CNS by bacterial compounds; and (3) possible direct toxicity of bacterial compounds on neurons. Neuronal injury is mediated by the release of reactive oxygen intermediates, proteases, cytokines and excitatory amino acids, and is executed by the activation of transcription factors, caspases and other proteases. In experimental meningitis, dexamethasone as an adjunct to antibiotic treatment leads to an aggravation of neuronal damage in the hippocampal formation, suggesting that corticosteroids might not be the ideal adjunctive therapy. Several approaches that interfere selectively with the mechanisms of neuronal injury are effective in animal models, including the use of nonbacteriolytic protein synthesis-inhibiting antibiotics, antioxidants and inhibitors of transcription factors, matrix metalloproteinases, and caspases.

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Metadata

Authors
Nau, R., & Brück, W.
Venue
Trends in Neurosciences
Publisher
Elsevier BV
Published
2002-01
Volume
25
Issue
1
Pages
38-45
ISSN
0166-2236 (ISSN-L)
OpenAlex
W1975663198
Cited by
291
References
78
FWCI
2.48
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Neuronal injury in bacterial meningitis: mechanisms and implications for therapy. https://app.cochat.ai/papers/10.1016/s0166-2236(00)02024-5
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Nau, R., & Brück, W. (2002). Neuronal injury in bacterial meningitis: mechanisms and implications for therapy. Trends in Neurosciences. https://doi.org/10.1016/s0166-2236(00)02024-5

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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