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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.
In the citing paper
“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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“Additionally, inflammation, which is a hallmark of AD pathology [48], and mitochondrial dysfunction can also contribute to DNA damage by generating reactive oxygen species (ROS) [5, 49].”
BackgroundTherapeutic Potential of PTB Inhibition Through Converting Glial Cells to Neurons in the Brain
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“Our data agree with emerging evidence that chronic inflammatory osteolysis contributes to neuroinflammation and dementia, indicating that chronic peripheral inflammation mediated by IL-34 may be a novel therapeutic target for AD [71–73].”
ResultShanks, H. R. C., Onuska, K. M., Massa, S. M., Schmitz, T. W., & Longo, F. M. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.110 · Cited by 17
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“Neuroinflammation caused by abnor - mal glial cells is found in mental disorders, such as stress and depression, and in several neurodegenerative diseases, such as PD and AD [35, 36].”
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“…bidirectional relationships between all these pathological concepts: disrupted sleep promotes low-grade inflammation and inflammation regulates sleep [6, 41, 55–58], whereas inflammation and disrupted sleep are thought of as both risk factors of AD and consequences of AD pathology [59, 60].”
BackgroundIanni, M., Corraliza-Gómez, M., Costa-Coelho, T., Ferreira-Manso, M., Inteiro-Oliveira, S., Alemãn-Serrano, N., Sebastião, A. M., Garcia, G., Diógenes, M. J., & Brites, D. M. T. O. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25179475 · Cited by 18
“This inflammation may contribute to the onset of AD or exacerbate amyloid and tau pathology [15].”
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“Chronic neuroinflammation is central to AD progression and is believed to contribute to cognitive impairment [5].”
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Chen, Z., Shi, J., & Li, L. (2025) · Advanced technology in neuroscience . · doi:10.4103/atn.atn-d-24-00015 · Cited by 16
Assessing the potential causal effects of 1099 plasma metabolites on 2099 binary disease endpoints
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A unified model of dementias and age‐related neurodegeneration
Fossel, M. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12012 · Cited by 16
Scarabino, D., Corbo, R. M., & Businaro, R. (2020) · Neural Regeneration Research · doi:10.4103/1673-5374.300986 · Cited by 16
“Novel potential markers of transit ion from MCI to AD include elevated levels of inflammatory cytokines (Kinney et al., 2018) and shortened leukocyte telomere length (LTL) (Scarabino et al., 2017).”
BackgroundVarinthra, P., Ganesan, K., Huang, S., Chompoopong, S., Eurtivong, C., Suresh, P., Wen, Z., & Liu, I. Y. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.615079 · Cited by 15
“Moreover, the brain areas other than the CA3-region and BLA are also affected by an enhanced inflammatory response in this transgenic ADmouse strain upon aging (Backman et al., 1999; Kinney et al., 2018).”
BackgroundLiu, L., Zou, M., Zeng, K., Ye, X., Wang, R., Wang, W., & Zhang, X. (2021) · Plant Foods for Human Nutrition · doi:10.1007/s11130-020-00874-4 · Cited by 16
“of AD pathologies or risk factors associated with AD and increases the severity of the disease [8, 9].”
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Tran, D. N., Bakx, A. T. C. M., van Dis, V., Aronica, E., Verdijk, R. M., & Ouwendijk, W. J. D. (2021) · Brain Pathology · doi:10.1111/bpa.13044 · Cited by 15
“Because neuroinflammation is a major contributor to neurodegeneration in AD [42], we hypothesized that inflammatory cells rather than HSV replication itself could be associated with specific AD- related pathological changes.”
BackgroundSabaie, H., Talebi, M., Gharesouarn, J., Asadi, M. R., Jalaiei, A., Arsang‐Jang, S., Hussen, B. M., Taheri, M. N., Khoshnoud, R. J., & Rezazadeh, M. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.812169 · Cited by 15
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“Many findings suggested that neuroinflammation plays a key role in the development of the neuropathological changes seen in AD [52].”
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Light-based gamma entrainment with novel invisible spectral flicker stimuli
Hansen, L. S., Carstensen, M. S., Henney, M. A., Nguyen, N. M., Thorning‐Schmidt, M. W., Broeng, J., Petersen, P. M., & Andersen, T. (2024) · Scientific Reports · doi:10.1038/s41598-024-75448-4 · Cited by 17
Bartolić, M., Matošević, A., Maraković, N., Bušić, V., Roca, S., Vikić‐Topić, D., Sabljić, A., Bosak, A., & Gašo-Sokač, D. (2024) · Journal of Enzyme Inhibition and Medicinal Chemistry · doi:10.1080/14756366.2024.2431832 · Cited by 16
“…1 – 16 and ache is displayed in tables s4–s19. among the hydrazones derived from pyridine-4-carbaldehyde, the most potent ache inhibitor was 8, with 4-fluorophenylamine. although each of the two groups were represented by a small number of compounds, a certain trend in inhibition potency…”
InfluentialYue, C., Fu, Y., Zhao, Y., Ou, Y., Sun, Y., & Tan, L. (2024) · Brain Network Disorders · doi:10.1016/j.bnd.2024.10.006 · Cited by 17
Baldensperger, T., Preissler, M., & Becker, C. F. W. (2024) · RSC Chemical Biology · doi:10.1039/d4cb00221k · Cited by 17
Copeland, E. N., LeBlanc, P. J., Duarte‐Guterman, P., Fajardo, V. A., & MacPherson, R. E. K. (2025) · The Journal of Physiology · doi:10.1113/jp288032 · Cited by 16
“…a neurotrophic factor, may provide a link between sarcopenic obesity and AD as it has been shown to be lower in patients with AD (Ng et al., 2019), sarcopenia (Miyazaki et al., 2021) and those living with obesity (Craft et al., 1993; Hong & Choi, 2020; Kinney et al., 2018; Luchsinger et al., 2004).”
Roig-Soriano, J., Edo, Á., Verdés, S., Martín-Alonso, C., Sánchez‐de‐Diego, C., Rodríguez-Estévez, L., Serrano, A. L., Abraham, C. R., Bosch, A., Ventura, F., et al. (2025) · Molecular Therapy · doi:10.1016/j.ymthe.2025.02.030 · Cited by 16
Lifestyle factors and plasma biomarkers of Alzheimer's disease: A narrative review
Hooper, C., Coley, N., Delrieu, J., & Guyonnet, S. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2025.100130 · Cited by 15
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“65 Increase in key indicators of inflammation like IL-6 and TNF-α, may impair the function of neurons and increase the risk of oxidative stress-related neuronal apoptosis.”
Type I interferons in health and disease: molecular aspects and clinical implications
Mavragani, C. P., & Crow, M. K. (2025) · Physiological Reviews · doi:10.1152/physrev.00047.2024 · Cited by 16
Lahariya, R., Anand, G., Kumari, B., & Priyadarshi, K. (2026) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2026.578870 · Cited by 20
Sukjamnong, S., Chen, H., Saad, S., & Santiyanont, R. (2022) · Toxicological Research · doi:10.1007/s43188-021-00114-0 · Cited by 14
“Traditional Thai herbal therapies may be an alternative treatment option for inflammation-related diseases, such as type 2 diabetes [18], cardiovascular diseases [19], rheumatoid arthritis [20], chronic inflammatory lung disease [21], asthma [22], and Alzheimer’s disease [23].”
BackgroundExperimental modelling of Alzheimer's disease for therapeutic screening
Blaikie, L., Kay, G., Maciel, P., & Lin, P. K. T. (2022) · European Journal of Medicinal Chemistry Reports · doi:10.1016/j.ejmcr.2022.100044 · Cited by 16
Chia, S. Y., Vipin, A., Ng, K. P., Tu, H., Bommakanti, A. S., Wang, B. Z., Tan, Y. J., Zailan, F. Z., Ng, A. S. L., Ling, S., et al. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220116 · Cited by 17
Carvalho, A., Barbosa, B. M., Flores, J. S., Gonçalves, P. D. C., Diniz, R., Cordeiro, Y., Fernández, C. O., Cukierman, D. S., & Rey, N. A. (2022) · Journal of Inorganic Biochemistry · doi:10.1016/j.jinorgbio.2022.112033 · Cited by 15
Iban‐Arias, R., Trageser, K. J., Yang, E., Griggs, E., Radu, A., Naughton, S. X., Rahim, M. A., Oguchi, T., Raval, U., Palmieri, J., et al. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-221046 · Cited by 15
Wang, Y., & Liu, X. (2023) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2023/9935942 · Cited by 15
RetractedKefir as a therapeutic agent in clinical research: a scoping review
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Szala‐Rycaj, J., Szewczyk, A., Zagaja, M. P., Kaczmarczyk‐Ziemba, A., Maj, M., & Andres‐Mach, M. (2023) · Nutrients · doi:10.3390/nu15092041 · Cited by 16
Wongpun, J., Chanmanee, T., Tocharus, J., Chokchaisiri, R., Chaichompoo, W., Suksamrarn, A., & Tocharus, C. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.110181 · Cited by 15
Chou, O., Zhou, J.-D., Li, L., Chan, J., Satti, D., Chou, V., Wong, W., Lee, S.-R., Cheung, B., Tse, G., et al. (2023) · Journal of Alzheimer's Disease · doi:10.3233/jad-220111 · Cited by 13
Catalpol rescues cognitive deficits by attenuating amyloid β plaques and neuroinflammation
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Li, S., Sakurai, K., Ohgidani, M., Kato, T. A., & Hikida, T. (2023) · Molecular Brain · doi:10.1186/s13041-023-01047-5 · Cited by 16
“It has been reported that increased microglial activation causes neuroinflammation and impairs hippocampal neurogenesis, neuronal synaptic morphology, and synaptic plasticity [63, 64].”
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“Mounting and compelling evidence suggest that systemic inflammatory process may play a central role in the development of Alzheimer’s disease (AD) (McGeer and McGeer, 1998; Kuo et al., 2005; Holmes, 2013; Heppner et al., 2015; Kinney et al., 2018).”
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“This sustained inflammatory response exacerbates neuronal damage and contributes to disease progression in both conditions [22,23].”
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“Additionally, the molecular hallmarks intrinsic to ADRD, such as chro-nicinflammation, oxidative stress, and the accumulation of amyloid-beta (Aβ) and tau proteins, have been linked with dysregulated bone metabolism and elevated fracture risk [33, 34, 35, 36, 37, 38, 39, 40, 41].”
Glyceraldehyde-3-phosphate dehydrogenase is involved in the pathogenesis of Alzheimer's disease
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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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