Inflammatory S100A9 and S100A12 proteins in Alzheimer's disease
Abstract
Inflammation, insoluble protein deposition and neuronal cell loss are important features of the Alzheimer's disease (AD) brain. S100B is associated with the neuropathological hallmarks of AD where it is thought to play a role in neuritic pathology. S100A8, S100A9 and S100A12 comprise a new group of inflammation-associated proteins that are constitutively expressed by neutrophils and inducible in numerous inflammatory cells. We investigated expression of S100B, S100A8, S100A9 and S100A12 in brain samples from sporadic and familial (PS-1) AD cases and controls using immunohistochemistry and Western blot analysis. S100B, S100A9 and S100A12, but not S100A8, were consistently associated with the neuropathological hallmarks of AD. Western blot analysis confirmed significant increases in soluble S100A9 in PS-1 AD compared to controls. S100A9 complexes that were resistant to reduction were also evident in brain extracts. A reactive component of a size consistent with hexameric S100A12 was seen in all cases. This study indicates a potential role for pro-inflammatory S100A9 and S100A12 in pathogenesis caused by inflammation and protein complex formation in AD.
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S100A12 is a pro-inflammatory protein localized within Aβ plaques.
“For instance, S100A12 is a pro‐inflammatory protein localized within Aβ plaques. 59 , 77”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [59]
S100A12 is a pro-inflammatory mediator that modulates neuroinflammation.
“DCUN1D5 is involved in the neddylation pathway that regulates protein homeostasis, 58 and S100A12 is a pro‐inflammatory mediator that modulates neuroinflammation. 59”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [59]
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References 70 · Cited by 161
- Authors
- Shepherd, C. E., Goyette, J., Utter, V., Rahimi, F., Yang, Z., Geczy, C. L., & Halliday, G. M.
- Affiliations
- Neuroscience Research Australia (AU)
- UNSW Sydney (AU)
- Uppsala University (SE)
- Corresponding author
- Shepherd, C.E.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2006-11
- Volume
- 27
- Issue
- 11
- Pages
- 1554-1563
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2004837900
- Cited by
- 161
- References
- 70
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 9 · 2023: 7 · 2022: 11 · 2021: 12 · 2020: 7 · 2019: 5 · 2018: 13 · 2017: 7 · 2016: 13 · 2015: 4 · 2014: 7 · 2013: 9 · 2012: 7
- FWCI
- 1.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- ANU Open Research (Australian National University) (submittedVersion)
- Funders
- University of Sydney
- Fondation pour la Recherche sur Alzheimer
- National Health and Medical Research Council
- National Institute on Alcohol Abuse and Alcoholism
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › S100 Proteins and Annexins
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, S100A9, S100A12, S100A8, S100B, neuroinflammation, familial Alzheimer's disease, sporadic Alzheimer's disease, amyloid plaques, neurofibrillary tangles, protein complexes
- MeSH terms
- S100A12 Protein, Aged, Aged, 80 and over, Aging, Alzheimer Disease, Brain, Brain Chemistry, Female, Humans, Male, Middle Aged, S100 Proteins, Neutrophils, Blotting, Western, Inflammation Mediators, Calgranulin B
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