The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Neuroinflammation Associated with Aging Sensitizes the Brain to the Effects of Infection or Stress
Open accessAbstract
The aging brain is characterized by a shift from the homeostatic balance of inflammatory mediators to a proinflammatory state. This increase in neuroinflammation is marked by increased numbers of activated and primed microglia, increased steady-state levels of inflammatory cytokines and decreases in anti-inflammatory molecules. These conditions sensitize the aged brain to produce an exaggerated response to the presence of an immune stimulus in the periphery or following exposure to a stressor. In the brain, proinflammatory cytokines can have profound effects on behavioral and neural processes. As the aged brain is primed to respond to inflammatory stimuli, infection or stress may produce more severe detriments in cognitive function in the aged. Typically after an immune stimulus, aged animals display prolonged sickness behaviors, increased cytokine induction and greater cognitive impairments compared to adults. Additionally, aging can also augment the central response to stressors leading to exaggerated cytokine induction and increased decrements in learning and memory. This alteration in neuroinflammation and resultant sensitization to extrinsic and intrinsic stressors can have considerable effects upon the elderly’s recovery and coping during disease and stress.
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Cites
From inflammation to sickness and depression: when the immune system subjugates the brain
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Self-citationChronic stress and age-related increases in the proinflammatory cytokine IL-6.
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Self-citationInterleukin-6 and risk of cognitive decline: MacArthur Studies of Successful Aging
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The impact of systemic infection on the progression of neurodegenerative disease
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Prior Stressor Exposure Sensitizes LPS-Induced Cytokine Production
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Cited by
CRP, IL-6 and depression: a systematic review and meta-analysis of longitudinal studies.
Valkanova, V., Ebmeier, K. P., & Allan, C. L. (2013) · Journal of Affective Disorders · doi:10.1016/j.jad.2013.06.004 · Cited by 972
Inflammation in schizophrenia: pathogenetic aspects and therapeutic considerations.
Müller, N. (2018) · Schizophrenia Bulletin · doi:10.1093/schbul/sby024 · Cited by 648
Mechanisms and treatment of late-life depression
Alexopoulos, G. S. (2019) · Translational Psychiatry · doi:10.1038/s41398-019-0514-6 · Cited by 592
Ng, A., Tam, W. W., Zhang, M. W., Ho, C. S., Husain, S. F., McIntyre, R. S., & Ho, R. C. (2018) · Scientific Reports · doi:10.1038/s41598-018-30487-6 · Cited by 572
The outdoor air pollution and brain health workshop
Block, M. L., Elder, A., Auten, R. L., Bilbo, S. D., Chen, H., Chen, J.-C., Cory-Slechta, D. A., Costa, D., Diaz-Sanchez, D., Dorman, D. C., et al. (2012) · NeuroToxicology · doi:10.1016/j.neuro.2012.08.014 · Cited by 539
Metadata
- Authors
- Sparkman, N. L., & Johnson, R. W.
- Venue
- Neuroimmunomodulation
- Publisher
- S. Karger AG
- Published
- 2008
- Volume
- 15
- Issue
- 4-6
- Pages
- 323-330
- ISSN
- 1021-7401 (ISSN-L)
- 1423-0216
- OpenAlex
- W1995997452
- Cited by
- 332
- References
- 11
- FWCI
- 10.86
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
