Association of Chronic Low-grade Inflammation With Risk of Alzheimer Disease in ApoE4 Carriers
Open accessAbstract
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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Some proinflammatory proteins in blood impact APOE genotypes differently for AD risk.
“As some proinflammatory proteins in blood impact APOE genotypes differently for AD risk [4, 20]”
From Blood PCSK9 Impacts Alzheimer's Disease Risk in an <i>APOE</i> Genotype‐Dependent Manner: A Prospective Cohort Study (2026) · cites this paper as [20]
The Results report that elevated blood C-reactive protein (CRP) was linked to increased Alzheimer disease risk in ApoE4 carriers, a pattern not observed in ApoE2 or ApoE3 carriers. This supports a genotype-dependent association, but the paper examines CRP rather than multiple proteins and does not establish that it causally impacts risk. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe inflammatory phenotype in resting APOE4 iAstrocytes could explain the mechanistic link between chronic inflammation and AD pathogenesis in APOE4 carriers.
“Our findings of an inflammatory phenotype in resting APOE4 iAstrocytes could explain the mechanistic link between chronic inflammation and AD pathogenesis in APOE4 carriers (Tao et al., 2018).”
From APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytes (2022) · cites this paper as Tao et al., 2018
The Results and Discussion report an association between chronic low-grade inflammation and increased Alzheimer disease risk in ApoE4 carriers, supporting the link the citing authors invoke. But the Discussion explicitly says the mechanism for that interaction is unknown, so this source does not establish a mechanistic link. The iAstrocyte finding is the citing authors’ own finding, not one attributed to Tao et al. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIn APOE4 carriers, chronic inflammation has been linked to an accelerated onset of AD symptoms.
“In APOE4 carriers, chronic inflammation has been linked to an accelerated onset of AD symptoms [77].”
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“C Reactive Protein Values for CRP above 3 mg/L were excluded as they were considered to reflect low-grade inflammation [47].”
BackgroundLiang, T., Hang, W., Chen, J., Wu, Y., Wen, B., Xu, K., Ding, B., & Chen, J. (2021) · Cell & Bioscience · doi:10.1186/s13578-021-00563-y · Cited by 54 · see citing works
Naler, L. B., Hsieh, Y.-P., Geng, S., Zhou, Z., Li, L., & Lu, C. (2022) · Communications Biology · doi:10.1038/s42003-022-03035-2 · Cited by 55 · see citing works
Hegazy, S. H., Thomassen, J. Q., Rasmussen, I. J., Nordestgaard, B. G., Tybjærg‐Hansen, A., & Frikke‐Schmidt, R. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12568 · Cited by 56 · see citing works
Walker, K. A., Gross, A. L., Moghekar, A., Soldan, A., Pettigrew, C. A., Hou, X., Lu, H., Alfini, A. J., Bilgel, M., Miller, M. I., et al. (2020) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2020.01.006 · Cited by 51 · see citing works
“Consistent with previous work which suggests that inflammation and APOE ε4 allele possession may act synergistically to promote neurodegenerative changes and increase AD risk (Tao et al., 2018), our results indicate that APOE ε4 allele possession magnifies the association between inflammation and reduced network conne…”
ResultRelationships between Inflammation and Age-Related Neurocognitive Changes
Jin, R., Chan, A. K. Y., Wu, J., & Lee, T. M. C. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232012573 · Cited by 54 · see citing works
“Previous research has also revealed that genetic susceptibility and chronic inflammation interaction in people with a high level of C-reactive protein (CRP; ≤ 8 mg/L), an indicator of inflammation states secreted in response to cytokines that indicates an increased risk of AD and of earlier disease onset [17].”
BackgroundZhang, Z., Na, H., Gan, Q., Tao, Q., Alekseyev, Y., Hu, J., Yan, Z., Yang, J. B., Tian, H., Zhu, S., et al. (2021) · Aging Cell · doi:10.1111/acel.13501 · Cited by 45 · see citing works
Self-citationTao, 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., et al. (2021) · Neurology · doi:10.1212/wnl.0000000000012512 · Cited by 45 · see citing works
“, high CRP levels).(3) Such inflammatory response may increase susceptibility to AD, especially among those already at risk (i.”
BackgroundSelf-citationRubinstein, T., Brickman, A. M., Cheng, B., Burkett, S., Park, H., Annavajhala, M. K., Uhlemann, A., Andrews, H., Gutierrez, J., Paster, B. J., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13683 · Cited by 45 · see citing works
Dvir-Szternfeld, R., Castellani, G., Arad, M., Cahalon, L., Colaiuta, S. P., Keren‐Shaul, H., Croese, T., Burgaletto, C., Baruch, K., Ulland, T. K., et al. (2021) · Nature Aging · doi:10.1038/s43587-021-00149-w · Cited by 42 · see citing works
Long, S., Chen, Y., Yi, M., Yang, Z., Wei, M., Li, T., Ni, J., Shi, J., & Tian, J. (2022) · Journal of Clinical Neuroscience · doi:10.1016/j.jocn.2022.11.016 · Cited by 44 · see citing works
APOE genetics influence murine gut microbiome
Zajac, D. J., Green, S. J., Johnson, L. A., & Estus, S. (2022) · Scientific Reports · doi:10.1038/s41598-022-05763-1 · Cited by 41 · see citing works
Insomnia symptom severity and cognitive performance: Moderating role of APOE genotype
Baril, A., Beiser, A., Sanchez, E., Mysliwiec, V., Redline, S. S., Gottlieb, D. J., O’Connor, G. T., Gonzales, M. M., Himali, D., Seshadri, S. S., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12405 · Cited by 47 · see citing works
Endothelial Progenitor Cells and Vascular Alterations in Alzheimer’s Disease
Custodia, A., Ouro, A., Romaus‐Sanjurjo, D., Peleteiro, J. M. P., de Vries, H. E., Castillo, J., & Sobrino, T. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.811210 · Cited by 45 · see citing works
Insulin resistance in Alzheimer’s disease: The genetics and metabolomics links
Amin, A. M., Mostafa, H. M. A., & Khojah, H. M. J. (2022) · Clinica Chimica Acta · doi:10.1016/j.cca.2022.12.016 · Cited by 45 · see citing works
Apolipoprotein E Effects on Mammalian Ovarian Steroidogenesis and Human Fertility
Oriá, R. B., de Almeida, J. Z., Moreira, C. N., Guerrant, R. L., & Figueiredo, J. R. (2020) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2020.06.003 · Cited by 43 · see citing works
Comorbidity‐driven multi‐modal subtype analysis in mild cognitive impairment of Alzheimer's disease
Katabathula, S., Davis, P. B., & Xu, R. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12792 · Cited by 43 · see citing works
Yamaguchi, S., Murakami, T., Satoh, M., Komiyama, T., Ohi, T., Miyoshi, Y., Endo, K., Hiratsuka, T., Hara, A., Tatsumi, Y., et al. (2023) · Neurology · doi:10.1212/wnl.0000000000207579 · Cited by 41 · see citing works
“In a previous study showing a cross-sectional association between chronic systemic inflammation and hippocampal volume, CRP ≥3 mg/L at ≥2 time points was defined as chronic low-grade inflammation.(41) Periodontitis is a chronic inflammation and increases CRP in severe cases(42); however, in this study, only 11 partici…”
BackgroundInflammation: A Major Target for Compounds to Control Alzheimer’s Disease
Maccioni, R. B., Navarrete, L. P., González, A., González-Canacer, A., Guzmán‐Martínez, L., & Cortés, N. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-191014 · Cited by 42 · see citing works
Crossing borders in Alzheimer’s disease: A T cell’s perspective
van Olst, L., Coenen, L., Nieuwland, J. M., Rodriguez-Mogeda, C., de Wit, N. M., Kamermans, A., Middeldorp, J., & de Vries, H. E. (2022) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2022.114398 · Cited by 44 · see citing works
The Role of Apolipoprotein E Isoforms in Alzheimer’s Disease
Roda, A. R., Montoliu‐Gaya, L., & Villegas, S. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180740 · Cited by 41 · see citing works
Association of CD14 with incident dementia and markers of brain aging and injury
Pase, M. P., Himali, J. J., Beiser, A., DeCarli, C. S., McGrath, E. R., Satizábal, C. L., Aparicio, H. J., Adams, H. H. H., Reiner, A. P., Longstreth, W. T., et al. (2019) · Neurology · doi:10.1212/wnl.0000000000008682 · Cited by 38 · see citing works
“SBP, mm Hg, mean (SD) 133 (19) 131 (20) 135 (21) 134 (22)”
Self-citationUchio, R., Muroyama, K., Okuda-Hanafusa, C., Kawasaki, K., Yamamoto, Y., & Murosaki, S. (2019) · Nutrients · doi:10.3390/nu11081822 · Cited by 38 · see citing works
“Previous reports have indicated that chronic low-grade inflammation is potentially associated with an increased risk of metabolic syndrome [7], atherosclerotic disease [8], Alzheimer’s disease [9], and cancer [10].”
BackgroundJun, G., You, Y., Zhu, C., Meng, G., Chung, J., Panitch, R., Hu, J., Xia, W., Bennett, D. A., Foroud, T., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12607 · Cited by 35 · see citing works
Self-citationLipids and brain inflammation in APOE4-associated dementia
Duro, M. V. V., Ebright, B., & Yassine, H. N. (2021) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000801 · Cited by 39 · see citing works
“The correlation between APOE4 and inflammation was clearly demonstrated in the Framingham cohort, where participants with APOE4 and elevated plasma C-reactive protein levels had a greater risk of developing AD dementia than age and sex-matched APOE2 and APOE3 carriers [60].”
BackgroundAssociation between inflammatory biomarkers and cognitive aging
Fang, Y., Doyle, M. F., Chen, J., Alosco, M. L., Mez, J. B., Satizábal, C. L., Qiu, W. Q., Murabito, J. M., & Lunetta, K. L. (2022) · PLoS ONE · doi:10.1371/journal.pone.0274350 · Cited by 38 · see citing works
Self-citationZhang, Z., Gan, Q., Han, J., Tao, Q., Qiu, W. Q., & Madri, J. A. (2023) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x231170041 · Cited by 36 · see citing works
Self-citationAltered SPMs and age‐associated decrease in brain DHA in APOE4 female mice
Martinsen, A., Tejera, N., Vauzour, D., Harden, G., Dick, J., Shinde, S., Barden, A. E., Mori, T. A., & Minihane, A. M. (2019) · The FASEB Journal · doi:10.1096/fj.201900423r · Cited by 35 · see citing works
“Neuroinflammation plays a key role in neuronal function and AD pathology (49).”
BackgroundAlzheimer's disease mechanisms in peripheral cells: Promises and challenges
Trushina, E. V. (2019) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1016/j.trci.2019.06.008 · Cited by 35 · see citing works
Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer’s Disease
Fülöp, T., Munawara, U., Larbi, A., Desroches, M., Rodrigues, S., Catanzaro, M., Guidolin, A., Khalil, A., Bernier, F., Barron, A. E., et al. (2020) · CNS Drugs · doi:10.1007/s40263-020-00737-1 · Cited by 32 · see citing works
Senescent accelerated prone 8 (SAMP8) mice as a model of age dependent neuroinflammation
Fernández, A., Quintana, E., Velasco, P., Moreno-Jimenez, B., de Andrés, B., Gaspar, M.-L., Liste, I., Vilar, M., Mira, H., & Cano, E. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02104-3 · Cited by 38 · see citing works
Uchio, R., Kawasaki, K., Okuda-Hanafusa, C., Saji, R., Muroyama, K., Murosaki, S., Yamamoto, Y., & Hirose, Y. (2021) · Nutrition Journal · doi:10.1186/s12937-021-00748-8 · Cited by 34 · see citing works
“Previous reports indicated that chronic low-grade inflammation is potentially associated with an increased risk of metabolic syndrome [7], atherosclerotic disease [8], Alzheimer’s disease [9], neurodegenerative disease [2], sickness behaviors and mood disturbance [10], cancer [11], and mortality [12, 13].”
BackgroundThe emerging role of brain neuroinflammatory responses in Alzheimer’s disease
AmeliMojarad, M., AmeliMojarad, M., & Cui, X. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1391517 · Cited by 34 · see citing works
Systemic inflammation as a moderator between sleep and incident dementia
Baril, A., Beiser, A., Redline, S. S., McGrath, E. R., Aparicio, H. J., Gottlieb, D. J., Seshadri, S. S., Pase, M. P., & Himali, J. J. (2020) · SLEEP · doi:10.1093/sleep/zsaa164 · Cited by 31 · see citing works
The Role of Chronic Infection in Alzheimer’s Disease: Instigators, Co-conspirators, or Bystanders?
Butler, L., & Walker, K. A. (2021) · Current Clinical Microbiology Reports · doi:10.1007/s40588-021-00168-6 · Cited by 30 · see citing works
Asthma amplifies dementia risk: Evidence from CSF biomarkers and cognitive decline
Nair, A. K., Hulle, C. A. V., Bendlin, B. B., Zetterberg, H., Blennow, K., Wild, N., Kollmorgen, G., Suridjan, I., Busse, W. W., & Rosenkranz, M. A. (2022) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12315 · Cited by 30 · see citing works
Botchway, B. O., Okoye, F. C., Chen, Y., Arthur, W. E., & Fang, M. (2022) · Aging and disease · doi:10.14336/ad.2021.0616 · Cited by 32 · see citing works
Wandering along the epigenetic timeline
Topart, C., Werner, E., & Arimondo, P. B. (2020) · Clinical Epigenetics · doi:10.1186/s13148-020-00893-7 · Cited by 34 · see citing works
“Chronic inflammation promotes numerous age-related pathologies, such as cance r [90] and neurodegenerative diseases [91, 92], hence the need to prevent it.”
BackgroundInflammatory and Pro-resolving Mediators in Frontotemporal Dementia and Alzheimer’s Disease
Fraga, V. G., Magalhaes, C. A., Loures, C. D. M. G., de Souza, L. C., Guimarães, H. C., Zauli, D. A. G., Ferriani, M. D. G. C., Ferreira, C. N., Caramelli, P., Sousa, L. P., et al. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2019.09.008 · Cited by 28 · see citing works
Mekli, K., Lophatananon, A., Maharani, A., Nazroo, J. Y., & Muir, K. R. (2023) · PLoS ONE · doi:10.1371/journal.pone.0288045 · Cited by 28 · see citing works
Biological brain age and resilience in cognitively unimpaired 70‐year‐old individuals
Marseglia, A., Dartora, C. M., Samuelsson, J., Poulakis, K., Mohanty, R., Shams, S., Lindberg, O. E., Rydén, L., Sterner, T. R., Skoog, J., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14435 · Cited by 27 · see citing works
“53,54 More recently, Hayek and coll.”
Oxytocin and elderly MRI-based hippocampus and amygdala volume: a 7-year follow-up study
Orihashi, R., Mizoguchi, Y., Imamura, Y., Yamada, S., Ueno, T., & Monji, A. (2020) · Brain Communications · doi:10.1093/braincomms/fcaa081 · Cited by 27 · see citing works
“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).”
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 · see citing works
Beyond the amyloid cascade: An update of Alzheimer's disease pathophysiology
Gouilly, D., Rafiq, M., Nogueira, L., Salabert, A., Payoux, P., Péran, P., & Pariente, J. (2023) · Revue Neurologique · doi:10.1016/j.neurol.2022.12.006 · Cited by 30 · see citing works
Myasoedova, E., Sattui, S. E., Lee, J., O'Brien, J. T., & Makris, U. E. (2024) · The Lancet Rheumatology · doi:10.1016/s2665-9913(24)00190-5 · Cited by 27 · see citing works
Fang, Y., Doyle, M. F., Alosco, M. L., Mez, J., Satizábal, C. L., Qiu, W. Q., Lunetta, K. L., & Murabito, J. M. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-215533 · Cited by 25 · see citing works
Self-citationMhatre‐Winters, I., Eid, A., Han, Y., Tieu, K., & Richardson, J. R. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23179829 · Cited by 26 · see citing works
“Importantly, this is consistent with clinical data from healthy individuals carrying the APOE3 or APOE4 gene; APOE4 females show a greater increase in both pro-inflammatory cytokine release and gene expression [82,85,86].”
ResultAyyubova, G., Kodali, M., Upadhya, R., Madhu, L. N., Attaluri, S., Somayaji, Y., Shuai, B., Rao, S., Shankar, G., & Shetty, A. K. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02971-y · Cited by 25 · see citing works
Abbatecola, A. M., Giuliani, A., Biscetti, L., Scisciola, L., Battista, P., Barbieri, M., Sabbatinelli, J., & Olivieri, F. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102257 · Cited by 22 · see citing works
Abdulhameed, N., Babin, A., Hansen, K. M., Weaver, R. R., Banks, W. A., Talbot, K., & Rhea, E. M. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01537-1 · Cited by 24 · see citing works
“Alzheimer’s disease (AD) is a progressive neurocognitive/ neurodegenerative disorder [1, 2] that leads to the most common type of dementia [3, 4].”
Low, A., Su, L., Stefaniak, J. D., Mak, E., Dounavi, M., Terrera, G. M., Ritchie, K. A., Ritchie, C. W., Markus, H. S., & O'Brien, J. T. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.10.029 · Cited by 26 · see citing works
Saleh, R. N. M., West, A. L., Ostermann, A. I., Schebb, N. H., Calder, P. C., & Minihane, A. M. (2021) · Frontiers in Nutrition · doi:10.3389/fnut.2021.723813 · Cited by 22 · see citing works
Zhao, X., Lu, J., Zhang, J., Liu, C., Wang, H., Wāng, Y., & Du, Q. (2024) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2024.107065 · Cited by 22 · see citing works
C-reactive protein: the nexus between inflammation and protein misfolding diseases
Roy, A., Zeller, J., Nero, T. L., Klepetko, J., Eisenhardt, S. U., Parker, M. W., McFadyen, J. D., & Peter, K. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1612703 · Cited by 22 · see citing works
Na, H., Yang, J. B., Zhang, Z., Gan, Q., Tian, H., Rajab, I. M., Potempa, L. A., Tao, Q., & Qiu, W. Q. (2023) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2023.02.013 · Cited by 27 · see citing works
Self-citationMechanisms 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 · see citing works
“99,100 This process activates glial cells, intensifying neuroinflammation.”
Kelliny, S., Zhou, X., & Bobrovskaya, L. (2025) · Journal of Neuroscience Research · doi:10.1002/jnr.70046 · Cited by 26 · see citing works
“Also, a chronic inflammatory state is linked to earlier onset of the disease in APOEε4 carriers (Tao et al. 2018).”
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 · see citing works
“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-citationHe, 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 · see citing works
Faraji, P., Kühn, H., & Ahmadian, S. (2024) · Journal of Molecular Neuroscience · doi:10.1007/s12031-024-02224-4 · Cited by 25 · see citing works
“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).”
BackgroundChen, X. R., Initiative, A. D. N., Shao, Y., & Sadowski, M. J. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210434 · Cited by 21 · see citing works
Statins for vascular dementia: A hype or hope
Raja, H. G., Al-Kuraishy, H. M., Shokr, M. M., Al-Gareeb, A. I., Al‐Harchan, N. A., Alruwaili, M., Papadakis, M., Alexiou, A. T., & Batiha, G. E. (2024) · Neuroscience · doi:10.1016/j.neuroscience.2024.12.059 · Cited by 21 · see citing works
“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 18 · see citing works
“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
- Venue
- JAMA Network Open
- Publisher
- American Medical Association (AMA)
- Published
- 2018-10-19
- Volume
- 1
- Issue
- 6
- Pages
- e183597
- ISSN
- 2574-3805 (ISSN-L)
- 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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