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Inflammation as a central mechanism in Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia‐related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms.
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“Numerous cytokines and chemokines have been shown to contribute to the pathogenesis of neurodegenerative diseases as summarized by the recent reviews.9,253,412”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [9]
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.
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“This immune response in turn activates glia and induces the secretion of pro-inflammatory cytokines, which can drive further aggregation of Aβ by affecting the capacity of microglia and astrocytes for phagocytosis and degradation [26].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [26]
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 microglial inflammation has been observed in the brains of AD patients at various disease stages, and pro-inflammatory cytokines such as IL-1β, IL-2, IL-6, and tumor necrosis factor-α have been shown to be upregulated in AD [35].”
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 [35]
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.
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“Aβ levels are generally well-correlated with immune activation indicated by microgliosis and astrocytosis [3].”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [3]
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
“Currently, the innate immune system activation, in particular microglia, is considered a contributing factor to AD pathogenesis rather than a consequence of pathology 2 .”
From ABI3 deletion in TgCRND8 mice is associated with reduced amyloid plaque pathology and altered glial response (2023) · cites this paper as [2]
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“Theses neuroinflammatory responses are considered a major driving factor in patients with neurodegeneration and Alzheimer’s disease pathology, which starts early in the course of the disease, prior to the formation of Aβ plaques in the brain73.”
From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [73]
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 the comparison between B6 and 5xFAD mice, the concentrations of two proinflammatory cytokines, interleukin-1 β (IL-1B), tumor necrosis factor-alpha (TNFα ), were increased Figure 3G), and those of two other cytokines, IL-10, IL-5, were decreased (Figure 3H), consistent with previous findings 30 .”
From Genetic variants of phospholipase C-γ2 alter the phenotype and function of microglia and confer differential risk for Alzheimer’s disease (2023) · cites this paper as [30]
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“Prolonged microglial activation may be detrimental, since it eventually leads to a self-perpetuating cycle involving the production of neurotoxic pro-inflammatory cytokines, damaging neurons, inducing more recruitment of microglia, further increasing their activation and release of pro-inflammatory cytokines [35].”
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 [35]
The cited source says what the claim attributes to it.
In the citing paper
“Neuroinflammation is also linked to neurodegeneration and neuronal loss, which are features that coincidently are associated with amyloid plaque formation (DeTure and Dickson, 2019; Kinney et al., 2018; Sung et al., 2020).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Kinney et al., 2018
In the citing paper
“Due to the dysregulation of GABAergic mechanism in AD, the inhibitory role of GABA on activated microglia is also lost which further contributes to the release of pro-inflammatory cytokines [17].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [17]
In the citing paper
“The chronic, sustained inflammatory response in the brain is considered the third core pathological feature of AD.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [84]
In the citing paper
“This chronic neuroinflammation is caused by persistent activation of glial cells and excessive release of cytotoxic molecules, which adversely affects brain function and is a major cofactor in the pathogenesis of many neurodegenerative disorders, including AD [84].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [84]
In the citing paper
“It provides a link between the other two core pathologies, Aβ plaques and NFTs [84].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [84]
In the citing paper
“Continuous activation of the brain’s immune cells, such as microglia, leads to the release and production of various proinflammatory cytokines, which aids tau and Aβ pathologies and leads to the loss of neurons [24].”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [24]
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Citations
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- Alzheimer's Impact Movement, 2017, Alzheimer's Disease Caregivers Factsheet
- 10.1186/1750-1326-9-20 · DOI · Paper page
- 10.1186/s13024-017-0216-6 · DOI · Paper page
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Khodabakhsh, P., Bazrgar, M., Dargahi, L., Mohagheghi, F., Taei, A. A., Parvardeh, S., & Ahmadiani, A. (2021) · Life Sciences · doi:10.1016/j.lfs.2021.120088 · Cited by 21
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“functional integrity, partly mediated by neuroinflammatory response [1-3].”
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“In addition, it has been found that giving stress-induced inulin to mice can significantly increase the content of SCFAs in the cecum, particularly acetate and propionate [159], while reducing pro-inflammatory cytokines and corticosterone levels associated with stress [165].”
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“…of b-amyloid (Ab) peptides into senile plaques (Brothers et al., 2018; Hampel et al., 2021); s-protein hyperphosphorylation into neurofibrillary tangles (Wegmann et al., 2021), oxidative stress (Rummel & Butterfield, 2021) and neuroinflammation (GuzmanMartinez et al., 2019; Kinney et al., 2018).”
BackgroundBi-Directional Relationship Between Autophagy and Inflammasomes in Neurodegenerative Disorders
Panda, C., & Mahapatra, R. K. (2022) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-021-01184-2 · Cited by 20
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“For example, genetic studies have identified gene variants of the microglial receptor TREM2 (triggering receptor expressed on myeloid cells 2) as risk factors for developing AD [6,7].”
BackgroundFares, S., Husseiny, W. M. E., Selim, K. B., & Massoud, M. A. M. (2023) · ACS Omega · doi:10.1021/acsomega.3c02051 · Cited by 22
Simple model systems reveal conserved mechanisms of Alzheimer’s disease and related tauopathies
Jiang, Y., & MacNeil, L. T. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00664-x · Cited by 22
Abdullahi, A., Wong, T. W. L., & Ng, S. S. M. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102202 · Cited by 21
Arjmand, S., Ilaghi, M., Sisakht, A. K., Guldager, M. B., Wegener, G., Landau, A. M., & GJEDDE, A. H. (2024) · Basic & Clinical Pharmacology & Toxicology · doi:10.1111/bcpt.14035 · Cited by 23
“11 Specifically, neuroinflammation exacerbates A β - and τ -pathologies, while A β - and τ -pathologies promote neuroinflammation, thus establishing a positive feedback loop.”
Vassal, M., Martins, F., Monteiro, B., Tambaro, S., Martínez‐Murillo, R., & Rebelo, S. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-04246-w · Cited by 24
“In particular, the continued release of pro-inflammatory cytokines from microglia exacerbates neuroinflammation and contributes to this buildup [234–236].”
A phase 2, open-label study of anti-inflammatory NE3107 in patients with dementias
Haroon, J. M., Jordan, K., Mahdavi, K. D., Rindner, E., Becerra, S. A., Surya, J. R., Zielinski, M. A., Venkatraman, V., Goodenowe, D. B., Hofmeister, K., et al. (2024) · Medicine · doi:10.1097/md.0000000000039027 · Cited by 20
“[1,4,5] 13] Therefore, anti-inflammatory and insulin-sensitizing drugs are being explored for their potential to slow AD progression and the associated cognitive decline.”
BackgroundInteraction of Cannabis Use and Aging: From Molecule to Mind
Yoo, H. B., DiMuzio, J. M., & Filbey, F. M. (2019) · Journal of Dual Diagnosis · doi:10.1080/15504263.2019.1665218 · Cited by 21
Chung, Y.-S., Choo, B. K. M., Ahmed, P. K., Othman, I., & Shaikh, M. F. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.00692 · Cited by 21
Khoury, R., & Grossberg, G. T. (2020) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2020.1790530 · Cited by 19
Puris, E., Auriola, S. O. K., Korhonen, P., Loppi, S. H., Kanninen, K. M., Malm, T., Koıstınaho, J., & Gynther, M. (2021) · Journal of Pharmaceutical Sciences · doi:10.1016/j.xphs.2021.08.013 · Cited by 19
Whole Blood Expression Pattern of Inflammation and Redox Genes in Mild Alzheimer’s Disease
Milanesi, E., Dobre, M., Cucos, C. A., Rojo, A. I., Jiménez-Villegas, J., Capetillo-Zarate, E., Matute, C., Piñol-Ripoll, G., Manda, G., & Cuadrado, A. (2021) · Journal of Inflammation Research · doi:10.2147/jir.s334337 · Cited by 20
“The critical role of neuroinflammation in the pathogenesis of AD is well documented by clinical and preclinical studies.(10) In response to local brain damages, a persistent immune response is elicited locally by various brain cells (resident macrophages – microglia, astrocytes, newly recruited myeloid cells, etc), an…”
BackgroundChu, J. M. T., Abulimiti, A., Wong, B. S., Zhao, G. D., Xiong, S. H., Zhao, M., Wang, Y., Chen, Y., Wang, J., Zhang, Y., et al. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.846631 · Cited by 19
“In post-mortem brains of AD patients, increase in these cytokines and their respective receptors are frequently observed and is correlated to the neuropathological changes in the hippocampal region (Kinney et al., 2018).”
BackgroundMohamad, H. E., Abo–Elmatty, D. M., Wahba, N. S., Shaheen, M. A., Sakr, R., & Wahba, A. S. (2022) · Life Sciences · doi:10.1016/j.lfs.2022.120613 · Cited by 20
TREM2 risk variants and associated endophenotypes in alzheimer’s disease
Dijkstra, J. I. R., Vermunt, L., Venkatraghavan, V., Ozhegov, G., Coomans, E. M., Ossenkoppele, R., van de Giessen, E., Hulsman, M., de Geus, C. M., van der Flier, W. M., et al. (2025) · Alzheimer's Research & Therapy · doi:10.1186/s13195-025-01700-2 · Cited by 18
Primary Cilia Structure Is Prolonged in Enteric Neurons of 5xFAD Alzheimer’s Disease Model Mice
Nguyen, V. T. T., Brücker, L., Volz, A.-K., Baumgärtner, J. C., dos Santos Guilherme, M., Valeri, F., May-Simera, H., & Endres, K. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222413564 · Cited by 16
“Inflammation is a central mechanism in AD with presence of a sustained immune response in the brain [28].”
BackgroundHan, C., Wang, J., Chen, Y., Guan, C.-P., Zhang, Y., & Wang, M. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1243588 · Cited by 18
From defense to disease: IFITM3 in immunity and Alzheimer's disease
Kehs, Z., Cross, A. C., & Li, Y. (2024) · Neurotherapeutics · doi:10.1016/j.neurot.2024.e00482 · Cited by 21
Recent Advances in Antibody Therapy for Alzheimer’s Disease: Focus on Bispecific Antibodies
Yang, H. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26136271 · Cited by 19
cGAS-STING signaling in Alzheimer's disease: Microglial mechanisms and therapeutic opportunities
Fazal, F., Dar, N. J., Ahamad, S., Khan, S., Bano, N., Saha, S., Nazir, A., & Bhat, S. A. (2026) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2025.101444 · Cited by 21
Mitochondrial biogenesis in organismal senescence and neurodegeneration
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Bonaterra‐Pastra, A., de Retana, S. F., Rivas-Urbina, A., Puig, N., Benı́tez, S., Pancorbo, O., Rodríguez‐Luna, D., Pujadas, F., Freijo, M. D. M., Tur, S., et al. (2021) · Biomedicines · doi:10.3390/biomedicines9010072 · Cited by 21
“Therefore, this finding could be related to the concept that inflammation is a central mechanism in the development of AD [65], which would be reflected at a systemic level in decreased anti-inflammatory capacity of HDL.”
BackgroundSava, A., Buron, F., Routier, S., Panainte, A. D., Bibire, N., & Profire, L. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111678 · Cited by 18
Gao, J., Wang, L., Zhao, C., Wu, Y., Lu, Z., Gu, Y., Ba, Z., Wang, X., Wang, J., & Xu, Y. (2021) · Journal of Leukocyte Biology · doi:10.1002/jlb.3ma0821-639rr · Cited by 18
Tung, M., Fung, K.-M., Hsu, H.-M., & Tseng, T. (2021) · RSC Advances · doi:10.1039/d1ra05311f · Cited by 18
The Neurocognitive Effects of Cannabis Across the Lifespan
Ellingson, J. M., Hinckley, J. D., Ross, J. M., Schacht, J. P., Bidwell, L. C., Bryan, A. D., Hopfer, C. J., Riggs, P., & Hutchison, K. E. (2021) · Current Behavioral Neuroscience Reports · doi:10.1007/s40473-021-00244-7 · Cited by 20
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The Convergence of Alzheimer’s Disease Pathogenesis Concepts
Kozin, S. A., & Makarov, A. А. (2019) · Molecular Biology · doi:10.1134/s0026893319060104 · Cited by 17
Luo, J. J., Wallace, W., & Kusiak, J. W. (2022) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2022.120294 · Cited by 17
Cai, M., Zhang, Y., Chen, S. X., Wu, Z., & Zhu, L. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.968444 · Cited by 20
Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways
Ibanez, K. R., McFarland, K. N., Phillips, J., Allen, M., Lessard, C. B., Zobel, L., De La Cruz, E. G., Shah, S., Vo, Q., Wang, X., et al. (2022) · Alzheimer's Research & Therapy · doi:10.1186/s13195-022-01044-1 · Cited by 18
Interaction Mechanism Between the HSV-1 Glycoprotein B and the Antimicrobial Peptide Amyloid-β
Bourgade, K., Frost, E. H., Dupuis, G., Witkowski, J. M., Laurent, B., Calmettes, C., Ramassamy, C., Desroches, M., Rodrigues, S., & Fülöp, T. (2022) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-220061 · Cited by 18
“However, several paradoxes forced us to expand this view of ACH and reconcile it with novel emerging data; for example: 1) A peptide deposition can occur in cognitively normal individuals [2–4]; 2) A peptides are abundant in the mild cognitive impairment stage of AD and decrease in some clinically diagnosed AD [5]; 3)…”
ResultThe β‐adrenergic hypothesis of synaptic and microglial impairment in Alzheimer's disease
Li, S. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.15782 · Cited by 18
“A large amount of clinical and experimental data from the past few decades has tied AD pathobiology tightly to the malfunctioning brain's innate immune system (Heneka et al., 2015; Kinney et al., 2018; Uddin et al., 2022).”
BackgroundLicinio, J., & Wong, M. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-01968-6 · Cited by 18
“Very briefly, it is known that neurodegenerative processes, including, but not limited to, AD, precipitate an inflammatory response in the brain [66].”
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“In AD, a proinflammatory state with widespread upregulation of cytokines and chemokines has been observed, and neuroinflammation is also implicated in the pathogenesis of amyloid plaques and neurofibrillary tangles [8].”
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Wang, J., Yu, Z., Ye, P., & Xu, B. (2023) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2023.109397 · Cited by 18
Tracing the Path between Mushrooms and Alzheimer’s Disease—A Literature Review
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“These can be combined with comple‐ mentary therapeutic approaches, such as anti‐inflammatory or antioxidant therapies, which are known to play an important role in neurodegeneration [13,14,26,40].”
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“Increased levels of proinflammatory IL-6 and TNF-α in brain tissues have been observed in patients with AD ( 53 , 54 ).”
Bludau, O., Weber, A., Bosak, V., Kuscha, V., Dietrich, K., Hans, S., & Brand, M. (2024) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2024.1332347 · Cited by 18
Mechanism of effect and therapeutic potential of NLRP3 inflammasome in spinal cord injury
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“18 In the context of the innate immune response, NLRP3 (nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing protein 3) inflammasome signaling within macrophages 19 and microglia 20 —specialized macrophages within the central nervous system (CNS)—leads to the release…”
Metadata
- Authors
- Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T.
- Affiliations
- University of Nevada, Las Vegas (US)
- Indiana University Indianapolis (US)
- Department of Psychology University of Nevada Las Vegas Las Vegas NV USA
- Corresponding author
- Kinney, Jefferson W.
- ORCID
- Lamb, Bruce T.
- Venue
- Alzheimer's & Dementia: Translational Research & Clinical Interventions
- Publisher
- Wiley
- Published
- 2018-01
- Volume
- 4
- Issue
- 1
- Pages
- 575-590
- ISSN
- 2352-8737 (ISSN-L)
- PMC
- PMC6214864
- OpenAlex
- W2889787710
- Cited by
- 2,253
- References
- 283
- Citations by year
- 2026: 187 · 2025: 395 · 2024: 401 · 2023: 353 · 2022: 326 · 2021: 286 · 2020: 226 · 2019: 76 · 2018: 1
- FWCI
- 13.95
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Alzheimer s & Dementia Translational Research & Clinical Interventions (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Digital Scholarship - UNLV (University of Nevada Reno) (submittedVersion, cc-by-nd)
- Digital Scholarship - UNLV (University of Nevada Reno) (submittedVersion, cc-by-nc-nd)
- IUScholarWorks (Indiana University) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institutes of Health (P20GM109025)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, neuroinflammation, microglia, amyloid plaques, neurofibrillary tangles, tau pathology, cytokines, risk factors, neurodegeneration
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