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Impact of C-Reactive Protein on Cognition and Alzheimer Disease Biomarkers in Homozygous APOE ɛ4 Carriers
Open accessAbstract
Background and objectives Previous research has shown that elevated blood C-reactive protein (CRP) is associated with increased Alzheimer disease (AD) risk only in APOE ε4 allele carriers; the objective of this study was to examine the interactive effects of plasma CRP and APOE genotype on cognition and AD biomarkers. Methods Data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study were analyzed, including APOE genotype; plasma CRP concentrations; diagnostic status (i.e., mild cognitive impairment and dementia due to AD); Mini-Mental State Examination (MMSE) and Clinical Dementia Rating Dementia Staging Instrument scores; CSF concentrations of β-amyloid peptide (Aβ 42 ), total tau (t-Tau) and phosphorylated tau (p-Tau); and amyloid (AV45) PET imaging. Multivariable regression analyses tested the associations between plasma CRP and APOE on cognitive and biomarker outcomes. Results Among 566 ADNI participants, 274 (48.4%) had no, 222 (39.2%) had 1, and 70 (12.4%) had 2 APOE ε 4 alleles. Among only participants who had 2 APOE ε4 alleles, elevated CRP was associated with lower MMSE score at baseline ( β [95% confidence interval] -0.52 [-1.01, -0.12]) and 12-month follow-up (β -1.09 [-1.88, -0.17]) after adjustment for sex, age, and education. The interaction of 2 APOE ε4 alleles and elevated plasma CRP was associated with increased CSF levels of t-Tau (β = 11.21, SE 3.37, p p APOE ε4 alleles, elevated CRP was associated with decreased CSF t-Tau and p-Tau. These effe…
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“our recent studies have shown that several proinflammatory proteins including C‐reactive protein (CRP) and MCP‐1 interact with APOE ε4 versus APOE ε2 in an opposite direction to impact AD risk [3, 4].”
From Blood PCSK9 Impacts Alzheimer's Disease Risk in an APOE Genotype‐Dependent Manner: A Prospective Cohort Study (2026) · cites this paper as [3]
In the citing paper
“Dementia diagnoses were made according to DSM‐IV criteria, based on longitudinal cognitive assessments, caregiver interviews, medical records, neuroimaging, and autopsy data when available.”
From Blood PCSK9 Impacts Alzheimer's Disease Risk in an APOE Genotype‐Dependent Manner: A Prospective Cohort Study (2026) · cites this paper as [3]
Citations
Cites
Imaging β-amyloid burden in aging and dementia
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Self-citationAssociation of Chronic Low-grade Inflammation With Risk of Alzheimer Disease in ApoE4 Carriers
Tao, Q., Ang, T. F. A., DeCarli, C., Auerbach, S. H., Devine, S., Stein, T. D., Zhang, X., Massaro, J., Au, R., & Qiu, W. Q. (2018) · JAMA Network Open · doi:10.1001/jamanetworkopen.2018.3597 · Cited by 239 · cited 2×
“, high CRP levels).(3) Such inflammatory response may increase susceptibility to AD, especially among those already at risk (i.”
BackgroundSelf-citationClinical application of apolipoprotein E genotyping to Alzheimer's disease
Roses, A., Strittmatter, W., Pericak-Vance, M., Corder, E., Saunders, A., & Schmechel, D. (1994) · The Lancet · doi:10.1016/s0140-6736(94)92960-2 · Cited by 125
Amyloid PET and cognitive decline in cognitively normal individuals: the SCIENCe project
Timmers, T., Ossenkoppele, R., Verfaillie, S. C. J., van der Weijden, C. W. J., Slot, R. E. R., Wesselman, L. M. P., Windhorst, A. D., Wolters, E. E., Yaqub, M., Prins, N. D., et al. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.02.020 · Cited by 63
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Tao, Q., Ang, T. F. A., Huang, J., Itchapurapu, I. S., Mez, J., Alosco, M., Au, R., Farrer, L. A., Zhang, X., Qiu, W. Q., et al. (2026) · Health Science Reports · doi:10.1002/hsr2.71810 · Cited by 1
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Metadata
- Authors
- Tao, Q., Alvin Ang, T. F., Akhter-Khan, S. C., Itchapurapu, I. S., Killiany, R., Zhang, X., Budson, A. E., Turk, K. W., Goldstein, L., Mez, J., Alosco, M. L., Qiu, W. Q., & Initiative, F. T. A. D. N.
- Affiliations
- King's College London (GB)
- From the Department of Pharmacology and Experimental Therapeutics (Q.T., I.S.I., W.Q.Q.), Framingham Heart Study (Q.T., T.F.A.A.), Department of Anatomy and Neurobiology (T.F.A.A., R.K.), Slone Epidemiology Center (T.F.A.A.), Department of Medicine (X.Z.), Department of Neurology (A.E.B., K.W.T., J.M., M.L.A.), Department of Psychiatry (W.Q.Q.), and Alzheimer's Disease and CTE Centers (A.E.B., K.W.T., L.G., J.M., M.L.A., W.Q.Q.), Boston University School of Medicine, MA; Department of Psychology (S...
- ORCID
- Venue
- Neurology
- Published
- 2021-09-21
- Volume
- 97
- Issue
- 12
- Pages
- e1243-e1252
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC8480484
- OpenAlex
- W3177794462
- Cited by
- 45
- References
- 5
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 9 · 2023: 13 · 2022: 7 · 2021: 2
- FWCI
- 5.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5u01ag024904-10)
- National Institute on Aging (U01-AG-024904)
- National Institute of Neurological Disorders and Stroke (K23NS102399)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- C-reactive protein, Alzheimer's disease, APOE ε4, inflammation, cognitive decline, mild cognitive impairment, dementia, total tau, phosphorylated tau, amyloid PET, cerebrospinal fluid biomarkers, genetic interactions, neurodegeneration
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