The DOI matches its Crossref record; 241 of the 244 references it cites were found in a registry or an index.
Neuroinflammation in Alzheimer's disease
Open accessAbstract
Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“since there is a strong correlation between immune activation and oxidative damage in neurodegenerative disease [42,43,44]”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [42]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Chronic low-grade inflammation contributes to both the onset and progression of AD and PD through microglial activation and pro-inflammatory cytokine release, accelerating neuronal injury [4].”
From What Are the Key Biological Pathways Through Which Lifestyle Factors Influence Neurodegeneration? (2025) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This aligns with biological evidence highlighting the roles of diet and circadian regulation in modulating neuroinflammation and glymphatic clearance [4,5].”
From What Are the Key Biological Pathways Through Which Lifestyle Factors Influence Neurodegeneration? (2025) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“During early stages of AD, microglia contribute to Αβ clearance15”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Converging lines of evidence from human genetics, neuroimaging and post-mortem brain tissue studies suggest that microglia are major contributors to molecular and phenotypic changes, including synaptic loss and Aβ clearance, in the AD brain [4].”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [4]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Likewise, microglia, the brain-resident immunocompetent macrophages, also recognize Aβ oligomers via receptors such as CD36, toll-like receptor 4 (TLR4) and TLR6 and triggering receptor expressed on myeloid cells 2 (TREM2), acquiring specific AD-associated phenotypes [14,15,16].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [14]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In AD, however, a subset of astrocytes undergoes reactive transformation, adopting inflammatory and metabolically altered states that compromise synaptic support and promote neurotoxicity (Heneka et al., 2015; Nassar et al., 2022).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In AD, these networks become maladaptive, leading to sustained inflammation, impaired synaptic support, defective myelination (Nasrabady et al.; 2018, Zhou et al., 2022), and breakdown of the blood-brain barrier (BBB), ultimately amplifying neurodegeneration (Heneka et al., 2015; Sweeney et al., 2018).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Receptors on microglia can bind Aβ fibrils, driving an inflammatory response similar to the M1 (proinflammatory) phenotype observed outside the central nervous system [84].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [84]
The cited source says what the claim attributes to it.
In the citing paper
“The reactive gliosis, encompassing microgliosis and astrogliosis, are prevalent neuropathological hallmarks observed in the brains of both human AD and mouse models of Aβ amyloidosis8,15,16.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [15]
The cited source says what the claim attributes to it.
In the citing paper
“Amyloid-associated gliosis is consistently observed in the brains of AD patients15 and amyloidosis mouse models8,16.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [15]
The cited source says what the claim attributes to it.
In the citing paper
“Increasing clinical evidence suggests that neuroinflammation functions as a vital factor in AD pathogenesis (2)”
From Understanding monocyte-driven neuroinflammation in Alzheimer’s disease using human cortical organoid microphysiological systems (2025) · cites this paper as [2]
The cited source says what the claim attributes to it.
In the citing paper
“altered microglial function has been implicated in the progression of AD”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, Aβ may initiate microglial activation, resulting in microglial migration to plaques, phagocytosis, and enzymatic degradation of Aβ [37].”
From Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy (2021) · cites this paper as [37]
The cited source says what the claim attributes to it.
In the citing paper
“Astrocytes become reactive and inflammatory, while microglia transition into chronically activated states that can amplify neuroinflammation (Heneka et al., 2015; Sofroniew and Vinters, 2010).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
The cited source says what the claim attributes to it.
In the citing paper
“Microglia, the brain's primary immune cells, play a dual and stage-dependent role in AD, initially contributing to Aβ clearance but transitioning into a chronically reactive, pro-inflammatory state under persistent pathological stress (Hansen et al., 2017; Heneka et al., 2015).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
The cited source says what the claim attributes to it.
In the citing paper
“Neuroinflammation is a prominent feature of the neuropathology of Alzheimer’s disease (AD), in addition to β-amyloid (Aβ) plaques, tau-containing neurofibrillary tangles (NFT), and synaptic dysfunction followed by neurodegeneration [1].”
From 25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner (2020) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“Emerging evidence indicates that neuroinflammation, mediated by activated glial cells, plays a fundamental role in the pathogenesis and neurodegeneration of AD [1].”
From 25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner (2020) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“While amyloid-β plaques and TAU tangles have long been recognized as pathological hallmarks of AD, emerging research highlights the critical role of neuroinflammation in disease progression [1, 35–37].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [35]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Galectin-3 (Gal-3) is a key protein involved in neuroinflammation and is strongly upregulated in neurodegenerative conditions16.”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [16]
Experimental — accuracy not yet measuredIn the citing paper
“Neuroinflammation is a common feature of AD9 and GWAS have associated several immune-related genes with AD including ABCA7, CD33, CLU, CR1, MS4A10, 11 and recently TREM2.12, 13”
From Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer's disease (2015) · cites this paper as [9]
In the citing paper
“Clinical evidence shows that TauO and brain inflammation also appear in the preclinical or prodromal AD stage, many decades prior to the onset of dementia. 100”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [100]
In the citing paper
“Furthermore, since the immune response exists throughout the pathological progress of AD [104, 105], suggesting that it may also participate in and aggravate the disease development.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [104]
In the citing paper
“Plaques were evident in multiple brain regions by 4mo in male and female 5xFAD mice, concomitant with the stereotypical activation and gliosis of plaque- and non-plaque-associated microglia (PAM and NPAM, respectively; Fig. 1A-C) [52, 53].”
From Microglia facilitate loss of perineuronal nets in the Alzheimer's disease brain (2020) · cites this paper as [52]
In the citing paper
“The neurotoxicity of microglial cells may also be related to their expression of tau, which is triggered by the deposition of Aβ in the brain and is known to be neurotoxic149.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [149]
In the citing paper
“In AD brains reactive microglia has been found colocalized with amyloid plaques. In addition, the reactive astrocytes accumulate around senile plaques next to the activated microglia (Heneka et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Heneka et al., 2015
In the citing paper
“The sustained exposure to cytokines, chemokines and Aβ, could be responsible for the functional impairment of microglial cells located around Aβ− deposits (Heneka et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Heneka et al., 2015
In the citing paper
“Microglial senescence can enhance the sensitivity of microglia to inflammatory stimuli; this phenomenon is called “priming” (Heneka et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Heneka et al., 2015
In the citing paper
“Popular neuroprotective strategies for AD management consist of discovering small molecules with the ability to block these Aβ interactions with intracellular and extracellular targets to avoid caspase activation and the expression of proapoptotic proteins, to reduce the stress kinase signaling cascades, to inhibit tau protein phosphorylation, to counterpoise cholinergic functional loss, and to bo”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [37]
In the citing paper
“The FDA has approved two drugs for mild cognitive impairment (MCI) to early, mild stages of AD after years of failed clinical trials. They are aducanemab, and lecanemab, among which aducanemab received accelerated approval [14, 15].”
From Current therapeutics for Alzheimer’s disease and clinical trials (2024) · cites this paper as [15]
In the citing paper
“Neuroinflammation and oxidative stress (OS) are undoubtedly hallmarks of neurodegeneration, contributing to disease progression.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [42]
In the citing paper
“These genetic findings are further supported by the common observation of aberrantly activated microglia in pathologically relevant AD brain regions, including within and surrounding Aβ plaques [59, 60].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [60]
In the citing paper
“Indeed, many of the risk genes associated with AD mediate their effects through microglia, the brain‐resident macrophages (Glass et al, 2010; Heneka et al, 2015; Nott et al, 2019).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Heneka et al, 2015
In the citing paper
“Neuroinflammation has been identified as a key contributor to the pathobiology of AD [2–4]”
In the citing paper
“and occurs at early disease stages [2, 5–7]”
In the citing paper
“Peripheral inflammation may exacerbate neuroinflammation [2].”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies
Lang, U. E., & Borgwardt, S. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350094 · Cited by 8,526
Glutamate neurotoxicity and diseases of the nervous system
Choi, D. W. (1988) · Neuron · doi:10.1016/0896-6273(88)90162-6 · Cited by 8,188
The chemokine system in diverse forms of macrophage activation and polarization
MANTOVANI, A., SICA, A., SOZZANI, S., ALLAVENA, P., VECCHI, A., & LOCATI, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.09.015 · Cited by 6,534
Iliff, J. J., Wang, M., Liao, Y., Plogg, B. A., Peng, W., Gundersen, G. A., Benveniste, H., Vates, G. E., Deane, R., Goldman, S. A., et al. (2012) · Science Translational Medicine · doi:10.1126/scitranslmed.3003748 · Cited by 5,824
MANTOVANI, A., SOZZANI, S., LOCATI, M., ALLAVENA, P., & SICA, A. (2002) · Trends in Immunology · doi:10.1016/s1471-4906(02)02302-5 · Cited by 5,528
Schroder, K., & Tschopp, J. (2010) · Cell · doi:10.1016/j.cell.2010.01.040 · Cited by 5,475
Astrocytes: Biology and pathology
Sofroniew, M. V., & Vinters, H. V. (2010) · Acta Neuropathologica · doi:10.1007/s00401-009-0619-8 · Cited by 5,196
Fate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages
Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M. F., Conway, S. J., Ng, L. G., Stanley, E. R., et al. (2010) · Science · doi:10.1126/science.1194637 · Cited by 5,175
Richness of human gut microbiome correlates with metabolic markers
Le Chatelier, E., Nielsen, T., Qin, J., Prifti, E., Hildebrand, F., Falony, G., Almeida, M., Arumugam, M., Batto, J.-M., Kennedy, S., et al. (2013) · Nature · doi:10.1038/nature12506 · Cited by 4,662
Querfurth, H. W., & LaFerla, F. M. (2010) · New England Journal of Medicine · doi:10.1056/nejmra0909142 · Cited by 4,569
Cited by
Sorted by citations
Items 601–700 of 1,118
Role of the Extracellular Matrix in Alzheimer’s Disease
Sun, Y., Xu, S., Jiang, M., Liu, X., Yang, L., Bai, Z., & Yang, Q. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.707466 · Cited by 119
Oligomeric Aβ in the monkey brain impacts synaptic integrity and induces accelerated cortical aging
Beckman, D., Ott, S., Donis-Cox, K., Janssen, W. G., Bliss-Moreau, E., Rudebeck, P. H., Baxter, M. G., & Morrison, J. H. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1902301116 · Cited by 111
Western, D., Timsina, J., Wang, L., Wang, C., Yang, C., Phillips, B., Wang, Y., Liu, M., Ali, M., Beric, A., et al. (2024) · Nature Genetics · doi:10.1038/s41588-024-01972-8 · Cited by 111
Self-citationCytokines and cytokine networks target neurons to modulate long-term potentiation
Prieto, G. A., & Cotman, C. W. (2017) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2017.03.005 · Cited by 118
Sifting through the surfeit of neuroinflammation tracers
Cumming, P., Burgher, B., Patkar, O., Breakspear, M., Vasdev, N., Thomas, P., Liu, G.-J., & Banati, R. (2018) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x17748786 · Cited by 111
Microglial interactions with the neurovascular system in physiology and pathology
Zhao, X., Eyo, U. B., Murugan, M., & Wu, L. (2018) · Developmental Neurobiology · doi:10.1002/dneu.22576 · Cited by 112
Theories of Aging and the Prevalence of Alzheimer’s Disease
Trevisan, K., Cristina-Pereira, R., Silva-Amaral, D., & Aversi‐Ferreira, T. A. (2019) · BioMed Research International · doi:10.1155/2019/9171424 · Cited by 120
Zheng, H., Liu, C.-C., Atagi, Y., Chen, X.-F., Jia, L., Yang, L., He, W., Zhang, X., Kang, S. S., Rosenberry, T. L., et al. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.03.004 · Cited by 110
Caruso, G., Caraci, F., & Jolivet, R. B. (2019) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2018.12.004 · Cited by 110
Precision pharmacology for Alzheimer’s disease
Hampel, H. J., Vergallo, A., Aguilar, L. F., Benda, N., Broich, K., Cuello, A. C., Cummings, J. L., Dubois, B., Federoff, H. J., Fiandaca, M. S., et al. (2018) · Pharmacological Research · doi:10.1016/j.phrs.2018.02.014 · Cited by 114
Invited Review: From nose to gut – the role of the microbiome in neurological disease
Bell, J. S., Spencer, J. I., Yates, R. L., Yee, S. A., Jacobs, B. M., & DeLuca, G. C. (2018) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12520 · Cited by 111
Systemic and CNS Inflammation Crosstalk: Implications for Alzheimer’s Disease
Paouri, E., & Georgopoulos, S. (2019) · Current Alzheimer Research · doi:10.2174/1567205016666190321154618 · Cited by 109
The Alzheimer's Disease Exposome
Finch, C. E., & Kulminski, A. M. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.06.3914 · Cited by 114
Predictive Value of Routine Peripheral Blood Biomarkers in Alzheimer’s Disease
Dong, X., Nao, J., Shi, J., & Zheng, D. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00332 · Cited by 110
Ullah, R., Ikram, M. A., Park, T. J., Ahmad, R., Saeed, K. M., Alam, S. I., Rehman, I. U., Khan, A., Khan, I., Jo, M. G., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms22010361 · Cited by 113
Testa, G., Gamba, P., Badıllı, U., Gargiulo, S., Maina, M., Guina, T., Calfapietra, S., Biasi, F., Cavalli, R., Poli, G., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0096795 · Cited by 114
Xu, H., Gelyana, E., Rajsombath, M., Yang, T., Li, S., & Selkoe, D. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.1023-16.2016 · Cited by 109
Suárez‐Calvet, M., Capell, A., Araque Caballero, M. Á., Morenas‐Rodríguez, E., Fellerer, K., Franzmeier, N., Kleinberger, G., Eren, E., Deming, Y., Piccio, L., et al. (2018) · EMBO Molecular Medicine · doi:10.15252/emmm.201809712 · Cited by 109
Hou, L., Sun, F., Huang, R., Sun, W., Zhang, D., & Wang, Q. (2019) · Redox Biology · doi:10.1016/j.redox.2019.101134 · Cited by 112
AlFadly, E. D., Elzahhar, P. A., Tramarin, A., Elkazaz, S., Shaltout, H. A., Abu-Serie, M. M., Janočková, J., Soukup, O., Ghareeb, D. A., EL‐Yazbi, A. F., et al. (2019) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2019.02.012 · Cited by 110
Microglial activation in early Alzheimer trajectory is associated with higher gray matter volume
Femminella, G. D., Dani, M., Wood, M., Fan, Z., Calsolaro, V., Atkinson, R., Edginton, T. L., Hinz, R., Brooks, D. J., & Edison, P. (2019) · Neurology · doi:10.1212/wnl.0000000000007133 · Cited by 109
Self-citationMast Cells in Neurodegenerative Disease
Jones, M. K., Nair, A. A., & Gupta, M. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00171 · Cited by 107
Vinuesa, Á., Pomilio, C. J., Gregosa, A., Bentivegna, M., Presa, J., Bellotto, M., Saravia, F., & Beauquis, J. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.653651 · Cited by 117
Inflammation and Alzheimer’s Disease: Mechanisms and Therapeutic Implications by Natural Products
Rather, M. A., Khan, A., Alshahrani, S., Rashid, H., Qadri, M. M., Rashid, S., Alsaffar, R. M., Kamal, M. A., & Rehman, M. U. (2021) · Mediators of Inflammation · doi:10.1155/2021/9982954 · Cited by 114
N-3 polyunsaturated fatty acids in animal models with neuroinflammation: An update
Trépanier, M., Hopperton, K. E., Orr, S. K., & Bazinet, R. P. (2015) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2015.05.045 · Cited by 114
Lactate metabolism in neurodegenerative diseases
Yang, C., Pan, R., Guan, F., & Yuan, Z. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.374142 · Cited by 115
DNA damage in the oligodendrocyte lineage and its role in brain aging
Tse, K.-H., & Herrup, K. (2017) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2016.05.006 · Cited by 108
Self-citationWoodling, N. S., Colas, D., Wang, Q., Minhas, P. S., Panchal, M., Liang, X., Mhatre, S. D., Brown, H. D., Ko, N., Zagol-Ikapitte, I. A., et al. (2016) · Brain · doi:10.1093/brain/aww117 · Cited by 111
Sarker, M. R., & Franks, S. F. (2018) · GeroScience · doi:10.1007/s11357-018-0017-z · Cited by 110
Meiner, Z., Ayers, E. I., & Verghese, J. (2020) · Annals of Geriatric Medicine and Research · doi:10.4235/agmr.20.0001 · Cited by 107
Baranowski, B. J., Marko, D. M., Fenech, R. K., Yang, A. J. T., & MacPherson, R. E. K. (2020) · Applied Physiology, Nutrition, and Metabolism · doi:10.1139/apnm-2019-0910 · Cited by 114
The effect of insomnia on development of Alzheimer’s disease
Sadeghmousavi, S., Eskian, M., Rahmani, F., & Rezaei, N. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01960-9 · Cited by 122
Targeting the NLRP3 inflammasome–IL-1β pathway in type 2 diabetes and obesity
Meier, D. T., Souza, J. D. P., & Donath, M. Y. (2024) · Diabetologia · doi:10.1007/s00125-024-06306-1 · Cited by 124
Pan, R.-Y., Zhang, J., Wang, J., Wang, Y., Li, Z., Liao, Y., Liao, Y., Zhang, C., Liu, Z., Song, L., et al. (2022) · Nature Aging · doi:10.1038/s43587-022-00311-y · Cited by 107
Subbarayan, M. S., Hudson, C., Moss, L. D., Nash, K. R., & Bickford, P. C. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01911-4 · Cited by 107
Mietelska‐Porowska, A., & Wojda, U. (2017) · Journal of Immunology Research · doi:10.1155/2017/4626540 · Cited by 111
Luo, Y., Kuang, S., Li, H., Ran, D., & Yang, J. (2017) · Oncotarget · doi:10.18632/oncotarget.16009 · Cited by 108
Diesel engine exhaust accelerates plaque formation in a mouse model of Alzheimer’s disease
Hullmann, M., Albrecht, C., van Berlo, D., Gerlofs-Nijland, M. E., Wahle, T., Boots, A. W., Krutmann, J., Cassee, F. R., Bayer, T. A., & Schins, R. P. F. (2017) · Particle and Fibre Toxicology · doi:10.1186/s12989-017-0213-5 · Cited by 107
Zádori, D., Veres, G., Szalárdy, L., Klivènyi, P., & Vécsei, L. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170929 · Cited by 108
Gene therapy for neurological disorders: challenges and recent advancements
Peña, S., Iyengar, R., Eshraghi, R. S., Bencie, N., Mittal, J., Aljohani, A., Mittal, R., & Eshraghi, A. A. (2019) · Journal of drug targeting · doi:10.1080/1061186x.2019.1630415 · Cited by 116
VDAC1 and the TSPO: Expression, Interactions, and Associated Functions in Health and Disease States
Shoshan‐Barmatz, V., Pittala, S., & Mizrachi, D. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20133348 · Cited by 112
Giacomeli, R., Izoton, J. C., dos Santos, R. B., Boeira, S. P., Jessé, C. R., & Haas, S. E. (2019) · Brain Research · doi:10.1016/j.brainres.2019.146325 · Cited by 109
Tondo, G., Iaccarino, L., Caminiti, S. P., Presotto, L., Santangelo, R., Iannaccone, S., Magnani, G., & Perani, D. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00619-0 · Cited by 109
Infectious disease-associated encephalopathies
Barbosa‐Silva, M. C., Lima, M. N., Battaglini, D., Robba, C., Pelosi, P. P., Rocco, P. R. M., & Maron‐Gutierrez, T. (2021) · Critical Care · doi:10.1186/s13054-021-03659-6 · Cited by 122
Nucleic acid drug vectors for diagnosis and treatment of brain diseases
Lü, Z., Shen, J., Yang, H. J., Wang, J., Zhao, R., Zhang, T.-L., Guo, J. R., & Zhang, X. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01298-z · Cited by 116
Alzheimer's disease outlook: controversies and future directions
Frisoni, G. B., Aho, E., Brayne, C., Ciccarelli, O., Dubois, B., Fox, N. C., Frederiksen, K. S., Gabay, C., Garibotto, V., Hofmarcher, T., et al. (2025) · The Lancet · doi:10.1016/s0140-6736(25)01389-3 · Cited by 116
Microglial large extracellular vesicles propagate early synaptic dysfunction in Alzheimer’s disease
Gabrielli, M., Prada, I., Joshi, P., Falcicchia, C., D’Arrigo, G., Rutigliano, G., Battocchio, E., Zenatelli, R., Tozzi, F., Radeghieri, A., et al. (2022) · Brain · doi:10.1093/brain/awac083 · Cited by 106
microRNA‐132: a key noncoding RNA operating in the cellular phase of Alzheimer's disease
Salta, E., & De Strooper, B. (2017) · The FASEB Journal · doi:10.1096/fj.201601308 · Cited by 99
Cinnamon, a promising prospect towards Alzheimer’s disease
Momtaz, S., Hassani, S., Khan, F., Ziaee, M., & Abdollahi, M. R. (2017) · Pharmacological Research · doi:10.1016/j.phrs.2017.12.011 · Cited by 108
A novel tau‐based rhesus monkey model of Alzheimer's pathogenesis
Beckman, D., Chakrabarty, P., Ott, S. P., Dao, A., Zhou, E., Janssen, W. G. M., Donis‐Cox, K., Muller, S., Kordower, J. H., & Morrison, J. H. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12318 · Cited by 112
Li, T., Lu, L., Pember, E., Li, X., Zhang, B., & Zhu, Z. (2022) · Cells · doi:10.3390/cells11121925 · Cited by 109
Miao, J., Chen, L., Pan, X., Li, L.-Q., Zhao, B., & Lan, J. X. (2023) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-023-01376-y · Cited by 121
Brain energy metabolism: A roadmap for future research
Rae, C. D., Baur, J. A., Borges, K., Dienel, G. A., Díaz‐García, C. M., Douglass, S. R., Drew, K. L., Duarte, J. M. N., Durán, J., Kann, O., et al. (2024) · Journal of Neurochemistry · doi:10.1111/jnc.16032 · Cited by 113
Zhao, N., Chen, Q.-G., Chen, X., Liu, X.-T., Geng, F., Zhu, M.-M., Yan, F.-L., Zhang, Z.-J., & Ren, Q.-G. (2023) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2022.11.013 · Cited by 105
Hernandez, M. X., Jiang, S., Cole, T. A., Chu, S., Fonseca, M. I., Fang, M. J., Hohsfield, L. A., Torres, M. D., Green, K. N., Wetsel, R. A., et al. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0210-z · Cited by 104
Kempuraj, D., Selvakumar, G. P., Thangavel, R., Ahmed, M. E., Zaheer, S. A., Raikwar, S. P., Iyer, S. S., Bhagavan, S., Ramaswamy, S. B., & Zaheer, A. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00703 · Cited by 108
Microglia in Alzheimer’s disease: A target for immunotherapy
Wang, S., & Colonna, M. (2019) · Journal of Leukocyte Biology · doi:10.1002/jlb.mr0818-319r · Cited by 106
Potential Neuroprotective Effect of the HMGB1 Inhibitor Glycyrrhizin in Neurological Disorders
Paudel, Y. N., Angelopoulou, E., Semple, B. D., Piperi, C., Othman, I., & Shaikh, M. F. (2020) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.9b00640 · Cited by 107
Mullane, K., & Williams, M. J. (2020) · Biochemical Pharmacology · doi:10.1016/j.bcp.2020.113945 · Cited by 109
Prakash, P., Manchanda, P., Paouri, E., Bisht, K., Sharma, K., Rajpoot, J., Wendt, V., Hossain, A., Wijewardhane, P. R., Randolph, C. E., et al. (2025) · Immunity · doi:10.1016/j.immuni.2025.04.029 · Cited by 104
Kaji, S., Berghoff, S. A., Spieth, L., Schlaphoff, L., Sasmita, A. O., Vitale, S., Büschgens, L., Kedia, S., Zirngibl, M., Nazarenko, T., et al. (2024) · Immunity · doi:10.1016/j.immuni.2024.09.014 · Cited by 104
Microglia-targeting nanotherapeutics for neurodegenerative diseases
Zhao, N., Francis, N. L., Calvelli, H. R., & Moghe, P. V. (2020) · APL Bioengineering · doi:10.1063/5.0013178 · Cited by 104
Gee, M. S., Son, S. H., Jeon, S. H., Do, J., Kim, N., Ju, Y., Lee, S. J., Chung, E. K., Inn, K., Kim, N., et al. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00617-2 · Cited by 105
Joly‐Amado, A., Hunter, J., Quadri, Z., Zamudio, F., Rocha-Rangel, P., Chan, D., Kesarwani, A., Nash, K. R., Lee, D. C., Morgan, D., et al. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00997 · Cited by 105
Self-citationAlterations in the Gut-Microbial-Inflammasome-Brain Axis in a Mouse Model of Alzheimer’s Disease
Shukla, P. K., Delotterie, D. F., Xiao, J., Pierre, J. F., Rao, R., McDonald, M. P., & Khan, M. M. (2021) · Cells · doi:10.3390/cells10040779 · Cited by 105
Inflammasomes in neurological disorders — mechanisms and therapeutic potential
Ravichandran, K. A., & Heneka, M. T. (2024) · Nature Reviews Neurology · doi:10.1038/s41582-023-00915-x · Cited by 112
Self-citationBrain health and shared risk factors for dementia and stroke
Gardener, H. E., Wright, C. B., Rundek, T., & Sacco, R. L. (2015) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.195 · Cited by 109
Li, H., Liu, C.-C., Zheng, H., & Huang, T. Y. (2018) · Translational Neurodegeneration · doi:10.1186/s40035-018-0139-3 · Cited by 103
Innate Immunity Fights Alzheimer's Disease
Guillot‐Sestier, M., Doty, K. R., & Town, T. (2015) · Trends in Neurosciences · doi:10.1016/j.tins.2015.08.008 · Cited by 101
Self-citationInteractions between inflammation, sex steroids, and Alzheimer’s disease risk factors
Uchoa, M. F., Moser, V. A., & Pike, C. J. (2016) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2016.09.001 · Cited by 105
Inflammatory Cascade in Alzheimer’s Disease Pathogenesis: A Review of Experimental Findings
de Oliveira, J., Kucharska, E., Garcez, M. L., Rodrigues, M. S., Quevedo, J., Moreno‐González, I., & Budni, J. (2021) · Cells · doi:10.3390/cells10102581 · Cited by 110
Ouyang, Q., Liu, K., Zhu, Q., Deng, H., Le, Y., Ouyang, W., Yan, X., Zhou, W., & Tong, J. (2022) · Small · doi:10.1002/smll.202107534 · Cited by 94
Du, C., Feng, W., Dai, X., Wang, J., Geng, D., Li, X., Chen, Y., & Zhang, J. (2022) · Small · doi:10.1002/smll.202203031 · Cited by 104
Alzheimer's disease pathophysiology in the Retina
Gaire, B. P., Koronyo, Y., Fuchs, D.-T. S., Shi, H., Rentsendorj, A., Danziger, R., Vit, J., Mirzaei, N., Doustar, J., Sheyn, J., et al. (2024) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2024.101273 · Cited by 107
Ryan, S. M., & Kelly, A. M. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.03.007 · Cited by 106
Effects of Tea Catechins on Alzheimer’s Disease: Recent Updates and Perspectives
Ide, K., Matsuoka, N., Yamada, H., Furushima, D., & Kawakami, K. (2018) · Molecules · doi:10.3390/molecules23092357 · Cited by 103
Innate Immunity: A Common Denominator between Neurodegenerative and Neuropsychiatric Diseases
Novellino, F., Saccà, V., Donato, A., Zaffino, P., Spadea, M. F., Vismara, M. F. M., Arcidiacono, B., Malara, N., Presta, I., & Donato, G. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21031115 · Cited by 107
The hypothalamus for whole-body physiology: from metabolism to aging
Liu, T., Xu, Y., Yi, C., Tong, Q., & Cai, D. (2021) · Protein & Cell · doi:10.1007/s13238-021-00834-x · Cited by 109
Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease
Tan, Y., Zheng, Y., Xu, D., Sun, Z., Yang, H., & Yin, Q. (2021) · Cell & Bioscience · doi:10.1186/s13578-021-00592-7 · Cited by 100
Data-driven modelling of neurodegenerative disease progression: thinking outside the black box
Young, A. L., Oxtoby, N. P., Garbarino, S., Fox, N. C., Barkhof, F., Schott, J. M., & Alexander, D. C. (2024) · Nature reviews. Neuroscience · doi:10.1038/s41583-023-00779-6 · Cited by 120
Cummings, J. L., Atri, A., Sano, M., Zetterberg, H., Scheltens, P., Knop, F. K., Johannsen, P., Wichmann, C. A., Abschneider, R. M., Leon, T., et al. (2026) · The Lancet · doi:10.1016/s0140-6736(26)00459-9 · Cited by 110
Muszyński, P., Groblewska, M., Kulczyńska‐Przybik, A., Kułakowska, A., & Mroczko, B. (2017) · Current Neuropharmacology · doi:10.2174/1570159x15666170208124324 · Cited by 104
A phase II study repurposing atomoxetine for neuroprotection in mild cognitive impairment
Levey, A. I., Qiu, D., Zhao, L., Hu, W. T., Duong, D. M., Higginbotham, L. A., Dammer, E. B., Seyfried, N. T., Wingo, T. S., Hales, C. M., et al. (2021) · Brain · doi:10.1093/brain/awab452 · Cited by 106
Characterizing primary human microglia: A comparative study with myeloid subsets and culture models
Melief, J., Sneeboer, M. A. M., Litjens, M., Ormel, P. R., Palmen, S. J. M. C., Huitinga, I., Kahn, R. S., Hol, E. M., & de Witte, L. D. (2016) · Glia · doi:10.1002/glia.23023 · Cited by 106
Venkataraman, A. V., Kalk, N. J., Sewell, G. W., Ritchie, C. W., & Lingford-Hughes, A. R. (2016) · Alcohol and Alcoholism · doi:10.1093/alcalc/agw092 · Cited by 104
Magnetic resonance spectroscopy reveals abnormalities of glucose metabolism in the Alzheimer's brain
Mullins, R. J., Reiter, D. A., & Kapogiannis, D. (2018) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.530 · Cited by 98
Mori, T., Koyama, N., Tan, J., Segawa, T., Maeda, M., & Town, T. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.004280 · Cited by 103
Self-citationTreating Alzheimer's disease by targeting iron
Nikseresht, S., Bush, A. I., & Ayton, S. (2019) · British Journal of Pharmacology · doi:10.1111/bph.14567 · Cited by 98
Benfante, R., Lascio, S. D., Cardani, S., & Fornasari, D. (2019) · Aging Clinical and Experimental Research · doi:10.1007/s40520-019-01359-4 · Cited by 102
Regulation of Tissue Inflammation by 12-Lipoxygenases
Kulkarni, A., Nadler, J. L., Mirmira, R. G., & Casimiro, I. (2021) · Biomolecules · doi:10.3390/biom11050717 · Cited by 103
Iulita, M. F., Ower, A., Barone, C., Pentz, R., Gubert, P., Romano, C., Cantarella, R. A., Elia, F., Buono, S., Recupero, M., et al. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.05.001 · Cited by 99
Gerischer, L. M., Fehlner, A., Köbe, T., Prehn, K., Antonenko, D., Grittner, U., Braun, J., Sack, I., & Flöel, A. (2017) · NeuroImage Clinical · doi:10.1016/j.nicl.2017.12.023 · Cited by 101
Plescher, M., Seifert, G., Hansen, J. N., Bedner, P., Steinhäuser, C., & Halle, A. (2018) · Glia · doi:10.1002/glia.23318 · Cited by 108
Self-citationInflammatory cytokines in highly myopic eyes
Yuan, J., Wu, S., Wang, Y., Pan, S., Wang, P., & Cheng, L. (2019) · Scientific Reports · doi:10.1038/s41598-019-39652-x · Cited by 102
The gut microbiota–brain axis in neurological disorders
You, M., Chen, N., Yang, Y., Cheng, L., He, H., Cai, Y., Liu, Y., Liu, H., & Hong, G. (2024) · MedComm · doi:10.1002/mco2.656 · Cited by 113
Toader, C., Tătaru, C. P., Munteanu, O., Șerban, M., Covache-Busuioc, R.-A., Ciurea, A. V., & Enyedi, M. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252312613 · Cited by 112
Mortadza, S. A. S., Sim, J. A., Neubrand, V. E., & Jiang, L. (2017) · Glia · doi:10.1002/glia.23265 · Cited by 102
PDE4B as a microglia target to reduce neuroinflammation
Pearse, D. D., & Hughes, Z. A. (2016) · Glia · doi:10.1002/glia.22986 · Cited by 98
Nillert, N., Pannangrong, W., Welbat, J. U., Chaijaroonkhanarak, W., Sripanidkulchai, K., & Sripanidkulchai, B. (2017) · Nutrients · doi:10.3390/nu9010024 · Cited by 101
Metadata
- Authors
- Heneka, M. T., Carson, M. J., Khoury, J. E., Landreth, G. E., Brosseron, F., Feinstein, D. L., Jacobs, A. H., Wyss-Coray, T., Vitorica, J., Ransohoff, R. M., Herrup, K., Frautschy, S. A., Finsen, B., Brown, G. C., Verkhratsky, A., Yamanaka, K., Koistinaho, J., Latz, E., Halle, A., Petzold, G. C., Town, T., Morgan, D., Shinohara, M. L., Perry, V. H., Holmes, C., Bazan, N. G., Brooks, D. J., Hunot, S., Joseph, B., Deigendesch, N., Garaschuk, O., Boddeke, E., Dinarello, C. A., Breitner, J. C., Cole, G. M., Golenbock, D. T., & Kummer, M. P.
- Affiliations
- University of Bonn (DE)
- University of California, Riverside (US)
- Case Western Reserve University (US)
- German Center for Neurodegenerative Diseases (DE)
- University of Illinois Chicago (US)
- University of Münster (DE)
- Cleveland Clinic (US)
- Hong Kong University of Science and Technology (HK)
- University of California, Los Angeles (US)
- University of Southern Denmark (DK)
- University of Cambridge (GB)
- Ikerbasque (ES)
- RIKEN (JP)
- Center of Advanced European Studies and Research (DE)
- University of Southern California (US)
- Duke Medical Center (US)
- Southampton General Hospital (GB)
- Southern Health NHS Foundation Trust (GB)
- Louisiana State University (US)
- Hammersmith Hospital (GB)
- Centre National de la Recherche Scientifique (FR)
- Karolinska Institutet (SE)
- Max Planck Institute for Infection Biology (DE)
- University of Tübingen (DE)
- University Medical Center Groningen (NL)
- University of Colorado Denver (US)
- Douglas Mental Health University Institute (CA)
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Heneka, Michael T
- ORCID
- Heneka, Michael T
- Carson, Monica J
- Landreth, Gary E
- Brosseron, Frederic
- Feinstein, Douglas L
- Jacobs, Andreas H
- Ransohoff, Richard M
- Herrup, Karl
- Frautschy, Sally A
- Finsen, Bente
- Brown, Guy C
- Verkhratsky, Alexei
- Yamanaka, Koji
- Latz, Eicke
- Halle, Annett
- Petzold, Gabor C
- Shinohara, Mari L
- Perry, V Hugh
- Holmes, Clive
- Bazan, Nicolas G
- Brooks, David J
- Hunot, Stéphane
- Joseph, Bertrand
- Deigendesch, Nikolaus
- Garaschuk, Olga
- Boddeke, Erik
- Dinarello, Charles A
- Breitner, John C
- Golenbock, Douglas T
- Kummer, Markus P
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 14
- Issue
- 4
- Pages
- 388-405
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC5909703
- OpenAlex
- W2087243986
- Cited by
- 6,226
- References
- 244
- Citations by year
- 2026: 686 · 2025: 708 · 2024: 713 · 2023: 640 · 2022: 665 · 2021: 620 · 2020: 554 · 2019: 506 · 2018: 406 · 2017: 342 · 2016: 259 · 2015: 110
- FWCI
- 29.69
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ePrints Soton (University of Southampton) (acceptedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, other-oa)
- eScholarship (California Digital Library) (submittedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- HAL (submittedVersion, other-oa)
- Max Planck Digital Library (submittedVersion)
- Deposito de Investigacion Universidad de Sevilla (University of Seville) (submittedVersion, cc-by-nc-nd)
- DZNE Pub (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Funders
- Medical Research Council (MR/L010593/1)
- Japan Society for the Promotion of Science (26293208)
- National Institute on Aging (R21AG053884)
- National Institute of Neurological Disorders and Stroke (R01NS059005, R01NS076794)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, neuroinflammation, innate immunity, microglia, astrocytes, pattern recognition receptors, protein aggregation, misfolded proteins, inflammatory mediators, systemic inflammation, obesity, genetic risk factors, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Anti-Inflammatory Agents, Non-Steroidal, Astrocytes, Brain Injuries, Clinical Trials as Topic, Disease Models, Animal, Humans, Immunity, Innate, Immunization, Inflammation, Locus Coeruleus, Obesity, Phagocytosis, Risk Factors, Severity of Illness Index, Biomarkers, Protein Folding, Microglia, Disease Progression, Nootropic Agents, Inflammation Mediators
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
