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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.
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“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.
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“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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β-Amyloid Clustering around ASC Fibrils Boosts Its Toxicity in Microglia
Friker, L. L., Scheiblich, H., Hochheiser, I. V., Brinkschulte, R., Riedel, D., Latz, E., Geyer, M., & Heneka, M. T. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.02.025 · Cited by 191
“, 2014), rapidly triggers NLRP3 inflammasome activation (Halle et al., 2008; Kinney et al., 2018).”
BackgroundNagpal, R., Neth, B. J., Wang, S., Mishra, S. P., Craft, S., & Yadav, H. (2020) · EBioMedicine · doi:10.1016/j.ebiom.2020.102950 · Cited by 197
“Given the emerging role of neuroinflammation in dementia, cognition and AD [84-86], these microbial and metabolite modulations may be a potential mechanism contributing to the efficacy of MMKD in improving CSF AD biomarkers in these patients with MCI [24, 42].”
BackgroundRole of JAK/STAT in the Neuroinflammation and its Association with Neurological Disorders
Jain, M., Singh, M. K., Shyam, H., Mishra, A., Kumar, S., Kumar, A., & Kushwaha, J. K. (2021) · Annals of Neurosciences · doi:10.1177/09727531211070532 · Cited by 196
Shabbir, U., Arshad, M. S., Sameen, A., & Oh, D.-H. (2021) · Nutrients · doi:10.3390/nu13020690 · Cited by 191
Randomized placebo-controlled trial of the effects of aspirin on dementia and cognitive decline
Ryan, J. L., Storey, E., Murray, A. M., Woods, R. L., Wolfe, R. S., Reid, C. M., Nelson, M. R., Chong, T. T. ‐., Williamson, J. D., Ward, S. A., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000009277 · Cited by 184
Mitochondrial Dysfunction and Alzheimer’s Disease: Role of Microglia
Agrawal, I., & Jha, S. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00252 · Cited by 184
“Owing to the direct involvement of Aβ and tau plaques in AD pathology, recent studies have elucidated a central role of inflammation in the pathophysiology of AD (Kinney et al., 2018).”
BackgroundChen, X., & Mobley, W. C. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00446 · Cited by 179
Novel Therapeutic Approaches for Alzheimer’s Disease: An Updated Review
Yu, T.-W., Lane, H., & Lin, C. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22158208 · Cited by 190
“Glial activation is associated with the signaling pathways of apolipoprotein E (ApoE), thus triggering the receptor expressed on myeloid cells 2 (TREM2), Toll-like receptor (TLR), and colonystimulating factor-1 receptor (CSF1R) (Figure 1, panel A) [199].”
BackgroundPromoting Successful Cognitive Aging: A Ten-Year Update
Krivanek, T. J., Gale, S. A., McFeeley, B. M., Nicastri, C. M., & Daffner, K. R. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201462 · Cited by 189
“ter changes, and A and tau pathology [171, 172].”
BackgroundAlzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses
(2024) · aging and disease · doi:10.14336/ad.2023.0608 · Cited by 183
“Previous studies have shown that individuals with AD have elevated levels of inflammatory markers such as cytokines, chemokines, and acute-phase proteins in the brain and cerebrospinal fluid, indicating the presence of chronic low-grade inflammation in the brain [43, 44].”
BackgroundAlzheimer’s Disease: Exploring the Landscape of Cognitive Decline
Tenchov, R., Sasso, J. M., & Zhou, Q. A. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.4c00339 · Cited by 170
Li, C., Wang, N., Zheng, G., & Yang, L. (2021) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.1c14818 · Cited by 173
Feng, S., Wu, C., Zou, P., Deng, Q., Chen, Z., Li, M., Zhu, L., Li, F., Liu, T. C., Duan, R., et al. (2023) · Theranostics · doi:10.7150/thno.81951 · Cited by 174
“individuals in the US and is expected to increase with improved life expectancy [3].”
Mechanism and therapeutic potential of targeting cGAS-STING signaling in neurological disorders
Huang, Y., Liu, B., Sinha, S. C., Amin, S., & Gan, L. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00672-x · Cited by 164
“Sustained neuroin-flammation in response to pathogenic proteins through activation of immune cells, especially microglia, has been recognized as another hallmark of AD [38].”
BackgroundMolecular Mechanisms of Neuroinflammation in Aging and Alzheimer’s Disease Progression
Andronie-Cioară, F. L., Ardelean, A. I., Nistor-Cseppento, C. D., Jurcău, A., Jurcău, M. C., Pașcalău, N., & Marcu, F. M. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24031869 · Cited by 170
Retinal Degeneration and Alzheimer’s Disease: An Evolving Link
Ashok, A., Singh, N., Chaudhary, S., Bellamkonda, V., Kritikos, A. E., Wise, A. S., Rana, N. A., McDonald, D., & Ayyagari, R. V. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21197290 · Cited by 164
“In addition to deposits of Aβ and p-tau, inflammation is a prominent feature of AD brains [3,101,102].”
Mediterranean Diet, Alzheimer Disease Biomarkers, and Brain Atrophy in Old Age
Ballarini, T., Melo van Lent, D., Brunner, J., Schröder, A., Wolfsgruber, S., Altenstein, S., Brosseron, F., Buerger, K., Dechent, P., Dobisch, L., et al. (2021) · Neurology · doi:10.1212/wnl.0000000000012067 · Cited by 153
Kim, J., Lee, H.-J., Park, S. K., Park, J.-H., Jeong, H.-R., Lee, S.-J., Lee, H., Seol, E., & Hoe, H. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910637 · Cited by 166
MicroRNAs in Alzheimer's disease: Potential diagnostic markers and therapeutic targets
Liu, S., Fan, M., Zheng, Q., Hao, S., Yang, L., Xia, Q., Qi, C., & Ge, J. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.112681 · Cited by 158
Resveratrol Derivatives as Potential Treatments for Alzheimer’s and Parkinson’s Disease
Arbo, B. D., André‐Miral, C., Nasre‐Nasser, R. G., Schimith, L. E., dos Santos, M. G., da Costa-Silva, D. G., Muccillo-Baisch, A. L., & Hort, M. A. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00103 · Cited by 159
Neuroinflammation as a Factor of Neurodegenerative Disease: Thalidomide Analogs as Treatments
Jung, Y. J., Tweedie, D., Scerba, M. T., & Greig, N. H. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00313 · Cited by 156
“…BACE1 leads to increased γ-secretase-mediated cleavage of APP, which leads to the generation and accumulation of Aβ (reviewed in Cole and Vassar, 2008), which in turn leads to increased inflammation, to yield a positive feedback loop of increased pathology (Combs et al., 2001; Kinney et al., 2018).”
BackgroundXu, C., Wu, J. S., Wu, Y., Ren, Z., Yao, Y., Chen, G., Fang, E. F., Noh, J. H., Liu, Y., Wei, L., et al. (2021) · Theranostics · doi:10.7150/thno.62376 · Cited by 151
“evidence has shown that extracellular Aβ plaques are directly toxic to adjacent neurons [6], and soluble or aggregated Aβ can also induce inflammatory processes and secondary cell death [7].”
BackgroundKim, H. S., Kim, S., Shin, S. J., Park, Y. H., Nam, Y., Lee, K. W., Lee, K. W., Kim, S., Yang, H. D., Yang, H. D., et al. (2021) · Translational Neurodegeneration · doi:10.1186/s40035-021-00273-y · Cited by 168
Dourado, N. S., Souza, C. D. S., de Almeida, M. M. A., da Silva, A. B., dos Santos, B. L., da Silva, V. D. A., de Assis, A. M., da Silva, J. S., Souza, D. O., Costa, M. D. F. D., et al. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00119 · Cited by 159
“Excessive IL-1β production in the CNS, mainly by glial cells, is associated with neuroinflammation found in neurodegenerative processes.”
BackgroundInfluentialFabrício, D. D. M., Chagas, M. H. N., & Diniz, B. S. (2020) · Translational research · doi:10.1016/j.trsl.2020.01.002 · Cited by 153
Frontera, J. A., Boutajangout, A., Masurkar, A. V., Betensky, R. A., Ge, Y., Vedvyas, A., Debure, L., Moreira, A., Lewis, A., Huang, J., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12556 · Cited by 157
“Highest serum IL-6, pg/mL, median (IQR) 24(7-82)”
Therapeutic Strategies Targeting Amyloid-β in Alzheimer’s Disease
Pinheiro, L. M. V., & Faustino, C. M. C. (2019) · Current Alzheimer Research · doi:10.2174/1567205016666190321163438 · Cited by 144
Chalcone and its analogs: Therapeutic and diagnostic applications in Alzheimer’s disease
Thapa, P., Upadhyay, S. P., Suo, W. Z., Singh, V., Gurung, P., Lee, E. S., Sharma, R., & Sharma, M. (2021) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2021.104681 · Cited by 151
“Microglial activation and production of inflammatory mediators— Activation of glial cells (astrocytes, microglia) results in accumulation of proinflammatory molecules exacerbating Aβ and tau pathology among other factors and causes progressive neuronal damage [165].”
BackgroundAlzheimer’s disease phospholipase C-gamma-2 (PLCG2) protective variant is a functional hypermorph
Magno, L., Lessard, C. B., Martins, M., Lang, V., Cruz, P., Asi, Y., Katan, M., Bilsland, J., Lashley, T., Chakrabarty, P., et al. (2019) · Alzheimer's Research & Therapy · doi:10.1186/s13195-019-0469-0 · Cited by 143
Gupta, V. B., Chitranshi, N., den Haan, J., Mirzaei, M., You, Y., Lim, J. K. H., Basavarajappa, D. K., Godinez, A., Angelantonio, S. D., Sachdev, P. S., et al. (2020) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2020.100899 · Cited by 149
“hallmark feature of several age-related neurodegenerative disorders (Kinney et al., 2018).”
BackgroundIron, Neuroinflammation and Neurodegeneration
Ward, R. J., Dexter, D. T., & Crichton, R. R. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23137267 · Cited by 144
Optical coherence tomography angiography in preclinical Alzheimer’s disease
van de Kreeke, J. A., Nguyen, H., Konijnenberg, E., Tomassen, J., den Braber, A., ten Kate, M., Yaqub, M. M., van Berckel, B. N. M., Lammertsma, A. A., Boomsma, D. I., et al. (2019) · British Journal of Ophthalmology · doi:10.1136/bjophthalmol-2019-314127 · Cited by 141
Emerging links between cerebrovascular and neurodegenerative diseases—a special role for pericytes
Lendahl, U., Nilsson, P., & Betsholtz, C. (2019) · EMBO Reports · doi:10.15252/embr.201948070 · Cited by 148
“A consequence of the deterioration of pericytes and loss of BBB integrity is an increased influx of immune cells into the brain, which in turn drives inflammation, an important disease-promoting factor in neurodegenerative as well as cerebrovascular disease (for review see [100]).”
Homocysteine Induces Inflammation in Retina and Brain
Elsherbiny, N. M., Sharma, I., Kira, D., Alhusban, S., Samra, Y. A., Jadeja, R. N., Martin, P. M., Al‐Shabrawey, M., & Tawfik, A. M. (2020) · Biomolecules · doi:10.3390/biom10030393 · Cited by 143
“Various investigations demonstrated that sustained inflammatory response is evident in the brain of AD patients [63].”
BackgroundEwers, M., Biechele, G., Suárez‐Calvet, M., Sacher, C., Blume, T., Morenas‐Rodriguez, E., Deming, Y., Piccio, L., Cruchaga, C., Kleinberger, G., et al. (2020) · EMBO Molecular Medicine · doi:10.15252/emmm.202012308 · Cited by 133
“…neuroinflammation in AD are complex and heterogenous involving multiple pathways (e.g., IL6, IL-1b, and YKL-40) and several studies suggest that microglia activation can have adverse effects in AD (Llorens et al, 2017; Kinney et al, 2018; Gotzl et al, 2019; for review, see Butovsky & Weiner, 2018).”
BackgroundThe emerging role of exosomes in Alzheimer’s disease
Zhang, T., Ma, S., Lv, J., Wang, X., Afewerky, H. K., Li, H. R., & Lu, Y. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101321 · Cited by 141
Hariyanto, T. I., Putri, C., Arisa, J., Situmeang, R. F. V., & Kurniawan, A. (2020) · Archives of Gerontology and Geriatrics · doi:10.1016/j.archger.2020.104299 · Cited by 137
“(Kinney et al., 2018; Simone & Tan, 2011) These persistent inflammatory state of dementia patients may be the cause of the increased peripheral blood white blood cells (WBC) and neutrophil counts in dementia patients with COVID-19.”
Chen, C., Zhou, Y., Wang, H., Alam, A. M., Kang, S. S., Ahn, E. H., Liu, X., Jia, J., & Ye, K. (2021) · The EMBO Journal · doi:10.15252/embj.2020106320 · Cited by 138
“…genetic causes of AD, neuroinflammation is not typically thought to be causal on its own, but rather a result of one or more AD pathologies or risk factors associated with AD, and serves to increase the severity of the disease by exacerbating b -amyloid and tau accumulation (Kinney et al , 2018).”
The intersection of metformin and inflammation
Bharath, L. P., & Nikolajczyk, B. S. (2021) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00604.2020 · Cited by 134
Inflammation in Neurological Disorders: The Thin Boundary Between Brain and Periphery
Cervellati, C., Trentini, A., Pecorelli, A., & Valacchi, G. (2020) · Antioxidants and Redox Signaling · doi:10.1089/ars.2020.8076 · Cited by 140
New Insights Into Drug Discovery Targeting Tau Protein
Soeda, Y., & Takashima, A. (2020) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2020.590896 · Cited by 136
Protective genes and pathways in Alzheimer’s disease: moving towards precision interventions
Seto, M., Weiner, R. L., Dumitrescu, L., & Hohman, T. J. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00452-5 · Cited by 135
Aaldijk, E., & Vermeiren, Y. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101556 · Cited by 138
Pancreatic cancer is marked by complement-high blood monocytes and tumor-associated macrophages
Kemp, S. B., Steele, N. G., Carpenter, E. S., Donahue, K. L., Bushnell, G. G., Morris, A. H., The, S., Orbach, S. M., Sirihorachai, V. R., Nwosu, Z. C., et al. (2021) · Life Science Alliance · doi:10.26508/lsa.202000935 · Cited by 129
“…macrophages in pancreatic cancer Kemp et al. https://doi.org/10.26508/lsa.202000935 vol 4 | no 6 | e202000935 12 of 17 TREM2 has been extensively evaluated in Alzheimer’s disease, a neurodegenerative disease, which, like cancer, ismarked by a chronic inflammatory response (Kinney et al, 2018).”
BackgroundInfluentialPathological changes within the cerebral vasculature in Alzheimer’s disease: New perspectives
Fisher, R. A., Miners, J. S., & Love, S. (2022) · Brain Pathology · doi:10.1111/bpa.13061 · Cited by 133
Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease
Craig, C. F., Filippone, R. T., Stavely, R., Bornstein, J. C., Apostolopoulos, V., & Nurgali, K. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02354-1 · Cited by 124
Neuroprotective effects of ononin against the aluminium chloride-induced Alzheimer’s disease in rats
Chen, X., Zhang, M., Ahmed, M., Surapaneni, K. M., Veeraraghavan, V. P., & Arulselvan, P. (2021) · Saudi Journal of Biological Sciences · doi:10.1016/j.sjbs.2021.06.031 · Cited by 129
The promise of music therapy for Alzheimer's disease: A review
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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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