The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease
Abstract
Systemic inflammation is associated with sickness behaviour and signals pass from the blood to the brain via macrophage populations associated with the brain, the perivascular macrophages and the microglia. The amplitude, or gain, of this transduction process is critically dependent on the state of activation of these macrophages. In chronic neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, or prion disease the pathology is associated with a highly atypical inflammatory response, characterised by the activation of the macrophage populations in the brain: the cells are primed. Recent evidence suggests that systemic inflammation may impact on local inflammation in the diseased brain leading to exaggerated synthesis of inflammatory cytokines and other mediators in the brain, which may in turn influence behaviour. These interactions suggest that systemic infections, or indeed any systemic challenge that promotes a systemic inflammatory response, may contribute to the outcome or progression of chronic neurodegenerative disease.
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Exercise has been shown to induce conversion of M1-type to M2-type myeloid cells in adipose tissue macrophages and inhibit M1-type macrophage infiltration.
“The fact that exercise has been shown to induce a conversion of M1-type to M2-type myeloid cells in adipose tissue macrophages coupled with inhibition of M1-type macrophage infiltration support this hypothesis.120”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [120]
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- Authors
- Perry, V. H.
- Affiliations
- University of Southampton (GB)
- Corresponding author
- Perry, V.Hugh
- ORCID
- Perry, V.Hugh
- Venue
- Brain Behavior and Immunity
- Publisher
- Elsevier BV
- Published
- 2004-09
- Volume
- 18
- Issue
- 5
- Pages
- 407-413
- ISSN
- 0889-1591 (ISSN-L)
- OpenAlex
- W2118118182
- Cited by
- 560
- References
- 22
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 31 · 2023: 20 · 2022: 33 · 2021: 37 · 2020: 26 · 2019: 22 · 2018: 27 · 2017: 34 · 2016: 25 · 2015: 26 · 2014: 33 · 2013: 27 · 2012: 32
- FWCI
- 16.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Funders
- Wellcome Trust
- Research Councils UK
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- systemic inflammation, neuroinflammation, microglia, perivascular macrophages, sickness behavior, macrophage priming, inflammatory cytokines, Alzheimer's disease, Parkinson's disease, prion disease, systemic infection, blood-brain barrier
- MeSH terms
- Alzheimer Disease, Animals, Brain, Chronic Disease, Disease Models, Animal, Humans, Inflammation, Leukocytes, Mononuclear, Lymphocyte Activation, Macrophages, Mice, Inbred C57BL, Cytokines, Prion Diseases, Neurodegenerative Diseases, Mice
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