Cited by 240Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

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Association of Chronic Low-grade Inflammation With Risk of Alzheimer Disease in ApoE4 Carriers

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Tao, Qiushan, Ang, Ting Fang Alvin, DeCarli, Charles, Auerbach, Sanford H., Devine, Sheral, Stein, Thor D., Zhang, Xiaoling, Massaro, Joseph, Au, Rhoda, Qiu, Wei Qiao·2018·JAMA Network Open

DOI 10.1001/jamanetworkopen.2018.3597PMC PMC6324596

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Abstract

Importance: The association between peripheral inflammatory biomarkers and Alzheimer disease (AD) is not consistent in the literature. It is possible that chronic inflammation, rather than 1 episode of inflammation, interacts with genetic vulnerability to increase the risk for AD. Objective: To study the interaction between the apolipoprotein E (ApoE) genotype and chronic low-grade inflammation and its association with the incidence of AD. Design, Setting, and Participants: In this cohort study, data from 2656 members of the Framingham Heart Study offspring cohort (Generation 2; August 13, 1971-November 27, 2017) were evaluated, including longitudinal measures of serum C-reactive protein (CRP), diagnoses of incident dementia including AD, and brain volume. Chronic low-grade inflammation was defined as having CRP at a high cutoff level at a minimum of 2 time points. Statistical analysis was performed from December 1, 1979, to December 31, 2015. Main Outcomes and Measures: Development of AD and brain volumes. Results: Of the 3130 eligible participants, 2656 (84.9%; 1227 men and 1429 women; mean [SD] age at last CRP measurement, 61.6 [9.5] years) with both ApoE status and longitudinal CRP measurements were included in this study analysis. Median (interquartile range) CRP levels increased with mean (SD) age (43.3 [9.6] years, 0.95 mg/L [0.40-2.35 mg/L] vs 59.1 [9.6] years, 2.04 mg/L [0.93-4.75 mg/L] vs 61.6 [9.5] years, 2.21 mg/L [1.05-5.12 mg/L]; P < .001), but less so among those with ApoE4 alleles, followed by ApoE3 then ApoE2 genotypes. During the 17 years of follow-up, 194 individuals (7.3%) developed dementia, 152 (78.4%) of whom had AD. ApoE4 coupled with chronic low-grade inflammation, defined as a CRP level of 8 mg/L or higher, was associated with an increased risk of AD, especially in the absence of cardiovascular diseases (hazard ratio, 6.63; 95% CI, 1.80-24.50; P = .005), as well as an increased risk of earlier disease onset compared with ApoE4 carriers without chronic inflammation (hazard ratio, 3.52; 95% CI, 1.27-9.75; P = .009). This phenomenon was not observed among ApoE3 and ApoE2 carriers with chronic low-grade inflammation. Finally, a subset of 1761 individuals (66.3%) underwent brain magnetic resonance imaging, and the interaction between ApoE4 and chronic low-grade inflammation was associated with brain atrophy in the temporal lobe (β = -0.88, SE = 0.22; P < .001) and hippocampus (β = -0.04, SE = 0.01; P = .005), after adjusting for confounders. Conclusions and Relevance: In this study, peripheral chronic low-grade inflammation in participants with ApoE4 was associated with shortened latency for onset of AD. Rigorously treating chronic systemic inflammation based on genetic risk could be effective for the prevention and intervention of AD.

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Figure 1. Cumulative Rates of Dementia, Alzheimer Disease (AD), and Mortality Based on ApoE Alleles and Chronic Low-grade Inflammation A, Cumulative incidence of AD, dementia, and mortality. Individuals were divided into ApoE2, ApoE3, and ApoE4 genotypes. To define the absence and presence of chronic low-grade inflammation, C-reactive protein (CRP) cutoff levels at 2 measurement points are used to represent severity. The incident rates of AD, dementia, and mortality between those without and with different severity levels of chronic low-grade inflammation were compared by using the χ2 test. To convert CRP to nanomoles per liter, multiply by 9.524. aP < .05. bP < .01. cP < .001. dP = .08. B, Cumulative incidence of AD. Individuals were divided into ApoE2, ApoE3, and ApoE4 genotypes for CRP concentrations of 3 mg/L or lower, 3 mg/L or higher, and 8 mg/L or higher. The AD incident rates were compared among the 3 ApoE subgroups by using the χ2 test for each level of CRP concentration.CC BY · PubMed Central

Figure 2. Kaplan-Meier Analysis for Survival Free of Alzheimer Disease (AD), Dementia, and Mortality in the Context of ApoE Alleles and Chronic Low-grade Inflammation A, AD-free probability for ApoE2 (P = .32). B, AD-free probability for ApoE3 (P = .14). C, AD-free probability for ApoE4 (P = .009). D, Dementia-free probability for ApoE2 (P = .74). E, Dementia-free probability for ApoE3 (P = .06). F, Dementia-free probability for ApoE4 (P = .001). G, Survival probability for ApoE2 (P = .18). H, Survival probability for ApoE3 (P < .001). I, Survival probability for ApoE4 (P = .19). C-reactive protein (CRP) cutoff level of 10 mg/L or higher at a minimum of 2 time points was used to define chronic low-grade inflammation.CC BY · PubMed Central

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Protein phosphatase 2A and complement component 4 are linked to the protective effect of APOE ɛ2 for Alzheimer's disease
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Association between inflammatory biomarkers and cognitive aging
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Altered SPMs and age‐associated decrease in brain DHA in APOE4 female mice
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Curcuma longa extract improves serum inflammatory markers and mental health in healthy participants who are overweight: a randomized, double-blind, placebo-controlled trial
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Systemic inflammation as a moderator between sleep and incident dementia
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Alzheimer Disease: Recent Updates on Apolipoprotein E and Gut Microbiome Mediation of Oxidative Stress, and Prospective Interventional Agents
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Inflammatory and Pro-resolving Mediators in Frontotemporal Dementia and Alzheimer’s Disease
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“Alzheimer’s disease is related to inflammation and treating chronic systemic inflammation may be effective in the prevention and intervention of Alzheimer’s disease (Tao et al. , 2018).”
Alzheimer’s Disease Susceptibility Gene Apolipoprotein E (APOE) and Blood Biomarkers in UK Biobank (N = 395,769)
Ferguson, A., Tank, R., Lyall, L. M., Ward, J., Celis-Morales, C. A., Strawbridge, R. J., Ho, F. K. W., Whelan, C. D., Gill, J. M. R., Welsh, P. I., et al. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200338 · Cited by 26
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Self-citation
Sex and APOE Genotype Alter the Basal and Induced Inflammatory States of Primary Microglia from APOE Targeted Replacement Mice
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Result
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Comparing regional brain uptake of incretin receptor agonists after intranasal delivery in CD-1 mice and the APP/PS1 mouse model of Alzheimer’s disease
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“Alzheimer’s disease (AD) is a progressive neurocognitive/ neurodegenerative disorder [1, 2] that leads to the most common type of dementia [3, 4].”
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APOE Genotype Modifies the Plasma Oxylipin Response to Omega-3 Polyunsaturated Fatty Acid Supplementation in Healthy Individuals
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Sleep restriction promotes brain oxidative stress and inflammation, and aggravates cognitive impairment in insulin-resistant mice
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Peripheral apolipoprotein E proteins and their binding to LRP1 antagonize Alzheimer's disease pathogenesis in the brain during peripheral chronic inflammation
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Self-citation
Mechanisms of comorbidity between Alzheimer's disease and pain
Yao, K., Wang, S., Xu, Z., Fan, Z., Chen, Z., Jia, P., Tu, S., Liu, Y., Lin, X., Xu, Y., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14605 · Cited by 23
“99,100 This process activates glial cells, intensifying neuroinflammation.”
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“Also, a chronic inflammatory state is linked to earlier onset of the disease in APOEε4 carriers (Tao et al. 2018).”
The impact of increasing levels of blood C-reactive protein on the inflammatory loci SPI1 and CD33 in Alzheimer’s disease
Huang, J., Tao, Q., Ang, T. F. A., Farrell, J. J., Zhu, C., Wang, Y., Stein, T. D., Lunetta, K. L., Massaro, J. M., Mez, J., et al. (2022) · Translational Psychiatry · doi:10.1038/s41398-022-02281-6 · Cited by 21
“DISCUSSION The results of this study extend our previous finding that elevated CRP impacts AD risk among APOE ε4 carriers [8] and the wellestablished relationship between inflammation and AD [40–42].”
MethodResultSelf-citation
Association between inflammatory burden index and all-cause mortality in the general population aged over 45 years: Data from NHANES 2005–2017
He, C., Wu, D., Wei, X., Li, Y., Liao, Y., & Yang, D. (2023) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2023.10.006 · Cited by 22
Multiple Roles of Apolipoprotein E4 in Oxidative Lipid Metabolism and Ferroptosis During the Pathogenesis of Alzheimer’s Disease
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“In a medium-scale (some 2500 patients) epidemiological study, the impact of chronic low-grade peripheral inflammation in APOE4 allele carriers was tested on the onset of AD (Tao et al. 2018).”
Background
Segmented Linear Mixed Model Analysis Reveals Association of the APOE ɛ4 Allele with Faster Rate of Alzheimer’s Disease Dementia Progression
Chen, X. R., Initiative, A. D. N., Shao, Y., & Sadowski, M. J. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210434 · Cited by 22
Statins for vascular dementia: A hype or hope
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“A cohort study indicated that high levels of systemic inflammatory biomarkers hasten the development of AD (Tao et al., 2018) .”
The Prevalence and Risk Factors of Cerebral Microbleeds: A Community-Based Study in China
Luo, Q., Tang, H., Xu, X., Huang, J., Wang, P., He, G., Song, X., Huang, Y., Chen, S., Yan, F., et al. (2021) · Therapeutics and Clinical Risk Management · doi:10.2147/tcrm.s297708 · Cited by 17
“Also, APOE ε4 carriers were tended to produce a stronger neuroinflammatory responding to peripheral systemic inflammation.(28) CR1, a receptor for complement C3b/ C4b, is also a central or peripheral factor involving complement mediated inflammation.”
Background

Authors: 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.
Affiliations: Boston University (US)
University of California Davis Medical Center (US)
Corresponding author: Au, Rhoda
Qiu, Wei Qiao
ORCID: Tao, Qiushan
Ang, Ting Fang Alvin
DeCarli, Charles
Auerbach, Sanford H.
Stein, Thor D.
Zhang, Xiaoling
Massaro, Joseph
Au, Rhoda
Qiu, Wei Qiao
Venue: JAMA Network Open
Publisher: American Medical Association (AMA)
Published: 2018-10-19
Volume: 1
Issue: 6
Pages: e183597
ISSN: 2574-3805 (ISSN-L)
DOI: 10.1001/jamanetworkopen.2018.3597
PMC: PMC6324596
OpenAlex: W2896917224
Cited by: 239
References: 34
Citations by year: 2026: 19 · 2025: 38 · 2024: 40 · 2023: 33 · 2022: 38 · 2021: 32 · 2020: 26 · 2019: 13
FWCI: 13.87
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: JAMA Network Open (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Institutes of Health (n01hc25195-41-0-1)
National Institute on Aging (P30AG010129, K24AG050842, U01AG052409, R01AG054076)
National Heart, Lung, and Blood Institute (N01‐HC25195)
National Institute of Neurological Disorders and Stroke (R01NS017950)
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: Alzheimer's disease, low-grade inflammation, apolipoprotein E, APOE ε4 carriers, C-reactive protein, inflammatory markers, dementia incidence, brain volume, cardiovascular disease, Framingham Offspring cohort, APOE3, APOE2
MeSH terms: Adult, Aged, Aged, 80 and over, Alzheimer Disease, Brain, C-Reactive Protein, Chronic Disease, Female, Humans, Inflammation, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Risk Factors, Cohort Studies, Apolipoprotein E4

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Association of Chronic Low-grade Inflammation With Risk of Alzheimer Disease in ApoE4 Carriers

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