The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Understanding the Role of Systemic Inflammation in Alzheimer’s Disease
Abstract
Human and animal studies suggest that inflammation occurring outside the central nervous system (systemic inflammation) may play a key role in promoting neurodegeneration, Alzheimer's disease pathology, and cognitive decline in older adults. Systemic inflammation, which is marked by increased blood levels of circulating proinflammatory cytokines and chemokines, may occur as a result of events such as infection, chronic disease, and physical and psychological stress, but may also occur outside the context of these conditions as a result of subclinical processes such as cellular senescence. Proinflammatory cytokines within the body can promote a proinflammatory environment in the central nervous system by crossing the blood-brain barrier, signaling through endothelial cells or circumventricular organs, and by stimulating the vagus nerve, which signals the detection of inflammatory proteins via direct afferent connections to the brain stem. Through each of these routes, systemic inflammation is believed to induce reactive, proinflammatory microglia and astrocytic phenotypes which can promote tau hyperphosphorylation, β-amyloid oligomerization, complement activation, and the breakdown of neurotransmitters into potentially harmful bioactive metabolites. Together, these molecular changes are believed initiate or exacerbate neurodegenerative processes that can eventually lead to cognitive decline and dementia in vulnerable older adults.
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“In addition, not limited to neuroinflammatory response, systemic inflammation is currently beginning to be considered a contributor to AD development of AD [106, 107].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [107]
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Cites
Kynurenines in the mammalian brain: when physiology meets pathology
Schwarcz, R., Bruno, J. P., Muchowski, P. J., & Wu, H.-Q. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3257 · Cited by 1,530
Systemic inflammation during midlife and cognitive change over 20 years: The ARIC Study
Walker, K. A., Gottesman, R. F., Wu, A., Knopman, D. S., Gross, A. L., Mosley, T. H., Selvin, E., & Windham, B. G. (2019) · Neurology · doi:10.1212/wnl.0000000000007094 · Cited by 282
Self-citationCunningham, C., & Hennessy, E. (2015) · Alzheimer's Research & Therapy · doi:10.1186/s13195-015-0117-2 · Cited by 211
Midlife systemic inflammatory markers are associated with late-life brain volume: The ARIC study
Walker, K. A., Hoogeveen, R. C., Folsom, A. R., Ballantyne, C. M., Knopman, D. S., Windham, B. G., Jack, C. R., & Gottesman, R. F. (2017) · Neurology · doi:10.1212/wnl.0000000000004688 · Cited by 150
Self-citationWalker, K. A., Windham, B. G., Power, M. C., Hoogeveen, R. C., Folsom, A. R., Ballantyne, C. M., Knopman, D. S., Selvin, E., Jack, C. R., & Gottesman, R. F. (2018) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.03.031 · Cited by 93
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Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation
Chen, Y., & Yu, Y. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02853-3 · Cited by 516
“In addition, not limited to neuroinflammatory response, systemic inflammation is currently beginning to be considered a contributor to AD development of AD [106, 107].”
BackgroundPeripheral and central immune system crosstalk in Alzheimer disease — a research prospectus
Bettcher, B. M., Tansey, M. G., Dorothée, G., & Heneka, M. T. (2021) · Nature Reviews Neurology · doi:10.1038/s41582-021-00549-x · Cited by 427
Inflammatory Processes in Alzheimer’s Disease—Pathomechanism, Diagnosis and Treatment: A Review
Twarowski, B., & Herbet, M. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076518 · Cited by 489
Monteiro, A. R., Barbosa, D. J., Remião, F., & Silva, R. V. D. S. (2023) · Biochemical Pharmacology · doi:10.1016/j.bcp.2023.115522 · Cited by 375
Neuroprotective effect of SGLT2 inhibitors.
Pawlos, A., Broncel, M., Woźniak, E., & Gorzelak-Pabiś, P. (2021) · Molecules · doi:10.3390/molecules26237213 · Cited by 304
Metadata
- Authors
- Walker, K. A., Ficek, B. N., & Westbrook, R.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Walker, Keenan A.
- Venue
- ACS Chemical Neuroscience
- Publisher
- American Chemical Society (ACS)
- Published
- 2019-06-26
- Volume
- 10
- Issue
- 8
- Pages
- 3340-3342
- ISSN
- 1948-7193 (ISSN-L)
- OpenAlex
- W2954317829
- Cited by
- 259
- References
- 5
- Citations by year
- 2026: 26 · 2025: 37 · 2024: 59 · 2023: 43 · 2022: 29 · 2021: 47 · 2020: 15 · 2019: 3
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- ACS Chemical Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG027668)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- systemic inflammation, Alzheimer's disease, neuroinflammation, inflammatory cytokines, chemokines, blood-brain barrier, vagus nerve, microglial activation, astrocytes, tau hyperphosphorylation, amyloid oligomerization, complement activation, cellular senescence, cognitive decline, dementia, older adults
- MeSH terms
- Alzheimer Disease, Animals, Humans, Inflammation, Neuroimmunomodulation
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