CRP gene variation affects early development of Alzheimer's disease-related plaques
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INTRODUCTION: We used the Tampere Autopsy Study (TASTY) series (n = 603, age 0-97 yrs), representing an unselected population outside institutions, to investigate the pathogenic involvement of inflammation in Alzheimer's disease-related lesions. METHODS: We studied senile plaque (SP), neurofibrillary tangles (NFT) and SP phenotype associations with 6 reported haplotype tagging single nucleotide polymorphisms (SNPs) in the CRP gene. CRP and Aβ immunohistochemistry was assessed using brain tissue microarrays. RESULTS: In multivariate analyses (age- and APOE-adjusted), non-neuritic SP were associated with the high-CRP TA-genotype (3.0% prevalence) of rs3091244 and CA-genotype (10.8%) of rs3093075 compared to common genotypes. Conversely, the low-CRP C allele (39.3%) of rs2794521 reduced the risk of harbouring early non-neuritic SP, compared to the TT genotype. CRP haplotype TAGCC (high) associated with non-neuritic SP, whereas haplotype CCGCC offered protection. TT genotypes (high) of rs3091244 and rs1130864 were associated with CRP staining. There were no associations between SNPs or haplotypes and NFT. CRP staining of the hippocampal CA1/2 region correlated with Aβ staining. CONCLUSIONS: CRP gene variation affects early SP development in prodromal Alzheimer's disease, independent of APOE genotype.
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C-reactive protein (CRP) levels are majorly associated with ApoE genotype and the CSF amyloid levels.
“C- reactive protein (CRP) levels are majorly associated with ApoE genotype and the CSF amyloid levels [47].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [47]
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- Authors
- Kok, E., Alanne-Kinnunen, M., Isotalo, K., Luoto, T., Haikonen, S., Goebeler, S., Perola, M., Hurme, M. A., Haapasalo, H., & Karhunen, P. J.
- Affiliations
- Tampere University Hospital (FI)
- Wihuri Research Institute (FI)
- Finnish Institute for Health and Welfare (FI)
- University of Helsinki (FI)
- Corresponding author
- Kok, Eloise
- ORCID
- Venue
- Journal of Neuroinflammation
- Published
- 2011
- Volume
- 8
- Issue
- 1
- Pages
- 96
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3168418
- OpenAlex
- W2036216712
- Cited by
- 16
- References
- 38
- Citations by year
- 2026: 1 · 2023: 1 · 2021: 3 · 2020: 1 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 2 · 2013: 2 · 2012: 1
- FWCI
- 0.65
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Tampere University Institutional Repository (Tampere University) (publishedVersion)
- Tampere University Institutional Repository (Tampere University) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- Funders
- Foundation for Cardiovascular Research
- Yrjö Jahnssonin Säätiö
- Suomen Kulttuurirahasto
- Sydäntutkimussäätiö
- Tays
- Pirkanmaan Rahasto
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, C-reactive protein, CRP gene polymorphisms, amyloid plaques, neurofibrillary tangles, inflammation, prodromal Alzheimer's disease, amyloid-beta, haplotypes, apolipoprotein E, hippocampus
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Alzheimer Disease, Animals, Autopsy, C-Reactive Protein, Child, Child, Preschool, Genotype, Humans, Infant, Male, Middle Aged, Phenotype, Neurofibrillary Tangles, Polymorphism, Single Nucleotide, Microarray Analysis, Apolipoprotein E4, Young Adult
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