The DOI matches its Crossref record; 266 of the 266 references it cites were found in a registry or an index.
Microglia in Alzheimer's Disease: a Key Player in the Transition Between Homeostasis and Pathogenesis
Open accessAbstract
Immune activation accompanies the development of proteinopathy in the brains of Alzheimer's dementia patients. Evolving from the long-held viewpoint that immune activation triggers the pathological trajectory in Alzheimer's disease, there is accumulating evidence now that microglial activation is neither pro-amyloidogenic nor just a simple reactive process to the proteinopathy. Preclinical studies highlight an interesting aspect of immunity, i.e., spurring immune system activity may be beneficial under certain circumstances. Indeed, a dynamic evolving relationship between different activation states of the immune system and its neuronal neighbors is thought to regulate overall brain organ health in both healthy aging and progression of Alzheimer's dementia. A new premise evolving from genome, transcriptome, and proteome data is that there might be at least two major phases of immune activation that accompany the pathological trajectory in Alzheimer's disease. Though activation on a chronic scale will certainly lead to neurodegeneration, this emerging knowledge of a potential beneficial aspect of immune activation allows us to form holistic insights into when, where, and how much immune system activity would need to be tuned to impact the Alzheimer's neurodegenerative cascade. Even with the trove of recently emerging -omics data from patients and preclinical models, how microglial phenotypes are functionally related to the transition of a healthy aging brain towards progressive degenerative state remains unknown. A deeper understanding of the synergism between microglial functional states and brain organ health could help us discover newer interventions and therapies that enable us to address the current paucity of disease-modifying therapies in 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
“Reviews and experimental studies now increasingly describe Alzheimer’s neuroinflammation as a dynamic balance between protective and harmful microglial programs, with disease stage and local tissue environment determining whether immune activation is beneficial, insufficient, maladaptive, or toxic [13,19].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [13]
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
“Microglia may help contain amyloid plaques, phagocytose pathological material, support synapses, and limit inflammatory spread; yet they may also release pro-inflammatory mediators, promote complement-associated synapse loss, propagate neurotoxic signaling, and contribute to chronic tissue damage.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [13]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“more recent work suggests that microglial responses in Alzheimer’s disease are not uniformly harmful and cannot be reduced to a simple activated-versus-resting distinction [13,14].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“The central unresolved issue is that the same broad category of “microglial activation” can describe processes with opposite biological consequences.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [13]
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
Items 201–266 of 266
Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response
Pimenova, A. A., Herbinet, M., Gupta, I., Machlovi, S. I., Bowles, K. R., Marcora, E., & Goate, A. M. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.105217 · Cited by 120 · cited 1×
“Low levels of SPI1 expression is linked to delayed AD onset [169], and entirely removing SPI1 expression dampens homeostatic microglia responses in the brain and increases microglial apoptosis [171].”
BackgroundUltrastructural evidence of microglial heterogeneity in Alzheimer’s disease amyloid pathology
El Hajj, H., Savage, J. C., Bisht, K., Parent, M., Vallières, L., Rivest, S., & Tremblay, M.-È. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1473-9 · Cited by 119
Prokop, S., Miller, K. R., Labra, S. R., Pitkin, R. M., Hoxha, K., Narasimhan, S., Changolkar, L., Rosenbloom, A., Lee, V. M.-Y., & Trojanowski, J. Q. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02048-2 · Cited by 119
Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau
Rayaprolu, S., Higginbotham, L., Bagchi, P., Watson, C. M., Zhang, T., Levey, A. I., Rangaraju, S., & Seyfried, N. T. (2021) · Neuropsychopharmacology · doi:10.1038/s41386-020-00840-3 · Cited by 118 · cited 1×
“Interestingly, many of these plaqueassociated proteins are themselves secreted by microglia and astrocytes and, in most cases, they are very immunogenic [43, 44].”
BackgroundChikina, M. D., Zaslavsky, E., & Sealfon, S. C. (2015) · Bioinformatics · doi:10.1093/bioinformatics/btv015 · Cited by 118
Hippocampal expression of murine TNFα results in attenuation of amyloid deposition in vivo
Chakrabarty, P., Herring, A., Ceballos-Diaz, C., Das, P., & Golde, T. E. (2011) · Molecular Neurodegeneration · doi:10.1186/1750-1326-6-16 · Cited by 117
Self-citationHippocampal expression of murine IL-4 results in exacerbation of amyloid deposition
Chakrabarty, P., Tianbai, L., Herring, A., Ceballos-Diaz, C., Das, P., & Golde, T. E. (2012) · Molecular Neurodegeneration · doi:10.1186/1750-1326-7-36 · Cited by 116
Self-citationLong-Term Cognitive Outcomes After Sepsis: a Translational Systematic Review
Barichello, T., Sayana, P., Giridharan, V. V., Arumanayagam, A. S., Narendran, B., Giustina, A. D., Petronilho, F. C., Quevedo, J., & Dal‐Pizzol, F. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1048-2 · Cited by 115
The Alzheimer's Disease Anti-inflammatory Prevention Trial Research Group (2013) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2012.11.012 · Cited by 115
[ 11 C]PK11195 binding in Alzheimer disease and progressive supranuclear palsy
Passamonti, L., Rodríguez, P. V., Hong, Y. T., Allinson, K. S. J., Bevan-Jones, W. R., Williamson, D., Jones, P. S., Arnold, R., Borchert, R. J., Surendranathan, A., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005610 · Cited by 115
Alzheimer’s disease risk polymorphisms regulate gene expression in the ZCWPW1 and the CELF1 loci
Karch, C. M., Ezerskiy, L. A., Bertelsen, S., Alzheimer’s Disease Genetics Consortium (ADGC), & Goate, A. M. (2016) · PLoS ONE · doi:10.1371/journal.pone.0148717 · Cited by 111
Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk
Salih, D. A., Bayram, S., Guelfi, S., Reynolds, R. H., Shoai, M., Ryten, M., Brenton, J. W., Zhang, D., Matarin, M., Botia, J. A., et al. (2019) · Brain Communications · doi:10.1093/braincomms/fcz022 · Cited by 110
Fractalkine overexpression suppresses tau pathology in a mouse model of tauopathy
Nash, K. R., Lee, D. C., Hunt, J. B., Morganti, J. M., Selenica, M.-L., Moran, P., Reid, P., Brownlow, M., Guang-Yu Yang, C., Savalia, M., et al. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.12.011 · Cited by 108
Inflammaging 2018: An update and a model
Franceschi, C., Zaikin, A. A., Gordleeva, S., Ivanchenko, M., Bonifazi, F., Storci, G., & Bonafè, M. (2018) · Seminars in Immunology · doi:10.1016/j.smim.2018.10.008 · Cited by 105
Eikelenboom, P., Rozemüller, A. J. M., & Muiswinkel, F. L. V. (1998) · Experimental Neurology · doi:10.1006/exnr.1998.6920 · Cited by 98
Microglial activation occurs late during preclinical Alzheimer's disease
Streit, W. J., Braak, H., Del Tredici, K., Leyh, J., Lier, J., Khoshbouei, H., Eisenlöffel, C., Müller, W., & Bechmann, I. (2018) · Glia · doi:10.1002/glia.23510 · Cited by 98
Boutej, H., Rahimian, R., Thammisetty, S. S., Béland, L., Lalancette–Hébert, M., & Križ, J. (2017) · Cell Reports · doi:10.1016/j.celrep.2017.11.058 · Cited by 96
Montgomery, S. L., Mastrangelo, M. A., Habib, D., Narrow, W. C., Knowlden, S. A., Wright, T. W., & Bowers, W. J. (2011) · The American Journal of Pathology · doi:10.1016/j.ajpath.2011.07.001 · Cited by 96
Raghavan, N. S., Dumitrescu, L. C., Mormino, E. C., Mahoney, E. R., Lee, A., Gao, Y., Bilgel, M., Goldstein, D. B., Harrison, T. M., Engelman, C. D., et al. (2020) · JAMA Neurology · doi:10.1001/jamaneurol.2020.1760 · Cited by 91
Partial reduction of microglia does not affect tau pathology in aged mice
Bennett, R. E., Bryant, A., Hu, M., Robbins, A. B., Hopp, S. C., & Hyman, B. T. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1348-5 · Cited by 91
Haure-Mirande, J.-V., Wang, M., Audrain, M., Fanutza, T., Kim, S. H., Heja, S., Readhead, B., Dudley, J. T., Blitzer, R. D., Schadt, E. E., et al. (2019) · Molecular Psychiatry · doi:10.1038/s41380-018-0255-6 · Cited by 84
Integrating Gene and Protein Expression Reveals Perturbed Functional Networks in Alzheimer’s Disease
Canchi, S., Raao, B., Masliah, D., Rosenthal, S. B., Šášik, R., Fisch, K. M., Jager, P. L. D., Bennett, D. A., & Rissman, R. A. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.06.073 · Cited by 82
Are infections seeding some cases of Alzheimer’s disease?
Abbott, A. (2020) · Nature · doi:10.1038/d41586-020-03084-9 · Cited by 82
Interferon-γ induces progressive nigrostriatal degeneration and basal ganglia calcification
Chakrabarty, P., Ceballos‐Diaz, C., Lin, W.-L., Beccard, A., Jansen‐West, K. R., McFarland, N. R., Janus, C., Dickson, D. W., Das, P., & Golde, T. E. (2011) · Nature Neuroscience · doi:10.1038/nn.2829 · Cited by 81
Self-citationBenítez, D. P., Jiang, S., Wood, J. I., Wang, R., Hall, C. M., Peerboom, C., Wong, N. S. M., Stringer, K. M., Vitanova, K. S., Smith, V. C., et al. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00457-0 · Cited by 81
TLR5 decoy receptor as a novel anti-amyloid therapeutic for Alzheimer’s disease
Chakrabarty, P., Li, A., Ladd, T. B., Strickland, M. R., Koller, E. J., Burgess, J. D., Funk, C. C., Cruz, P. E., Allen, M., Yaroshenko, M., et al. (2018) · The Journal of Experimental Medicine · doi:10.1084/jem.20180484 · Cited by 80
Self-citationNonsteroidal anti-inflammatory drug use and Alzheimer's disease risk: the MIRAGE Study
Yip, A. G., Green, R. C., Huyck, M., Cupples, L. A., Farrer, L. A., & for the MIRAGE Study Group (2005) · BMC Geriatrics · doi:10.1186/1471-2318-5-2 · Cited by 79
Identification of conserved proteomic networks in neurodegenerative dementia
Swarup, V., Chang, T. S., Duong, D. M., Dammer, E. B., Lah, J. J., Johnson, E. E. C. B., Seyfried, N. T., Levey, A. I., & Geschwind, D. H. (2019) · doi:10.1101/825802 · Cited by 78
Identification of Conserved Proteomic Networks in Neurodegenerative Dementia
Swarup, V., Chang, T. S., Duong, D. M., Dammer, E. B., Dai, J., Lah, J. J., Johnson, E. C. B., Seyfried, N. T., Levey, A. I., & Geschwind, D. H. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.107807 · Cited by 78
Innate Immunity, Local Inflammation, and Degenerative Disease
McGeer, P. L., & McGeer, E. G. (2002) · Science of Aging Knowledge Environment · doi:10.1126/sageke.2002.29.re3 · Cited by 75
Enhancer variants associated with Alzheimer’s disease affect gene expression via chromatin looping
Kikuchi, M., Hara, N., Hasegawa, M., Miyashita, A., Kuwano, R., Ikeuchi, T., & Nakaya, A. (2019) · BMC Medical Genomics · doi:10.1186/s12920-019-0574-8 · Cited by 74 · cited 1×
“Variants also exert effects on transcript levels over a greater distance – greater than 1 Mb from the location of the SNP – and in AD almost 30% of non-coding variants reside in enhancer regions and are thought to act by modulating the higher-order chromatin structure [165].”
BackgroundNeuroinflammation and neurodegeneration in human brain at single-cell resolution
Colonna, M., & Brioschi, S. (2019) · Nature reviews. Immunology · doi:10.1038/s41577-019-0262-0 · Cited by 71
Lodder, C., Scheyltjens, I., Stancu, I., Lucena, P. B., de Ravé, M. G., Vanherle, S., Vanmierlo, T., Cremers, N., Vanrusselt, H., Brône, B., et al. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01204-8 · Cited by 71
Interleukin-10 deficiency exacerbates inflammation-induced tau pathology
Weston, L. L., Jiang, S., Chisholm, D., Jantzie, L. L., & Bhaskar, K. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02211-1 · Cited by 69
Audrain, M., Haure-Mirande, J.-V., Wang, M., Kim, S. H., Fanutza, T., Chakrabarty, P., Fraser, P., St George-Hyslop, P. H., Golde, T. E., Blitzer, R. D., et al. (2019) · Molecular Psychiatry · doi:10.1038/s41380-018-0258-3 · Cited by 68
Self-citationMerino, J. J., Muñetón‐Gómez, V. C., Álvarez, M., & Toledano‐Díaz, A. (2016) · Current Alzheimer Research · doi:10.2174/1567205013666151116125714 · Cited by 62
Montgomery, S. L., Narrow, W. C., Mastrangelo, M. A., Olschowka, J. A., O'Banion, M. K., & Bowers, W. J. (2013) · The American Journal of Pathology · doi:10.1016/j.ajpath.2013.02.030 · Cited by 58
Increased tauopathy drives microglia-mediated clearance of beta-amyloid
Chen, W., Abud, E., Yeung, S. T., Lakatos, A., Nassi, T., Wang, J., Blum, D. L., Buée, L., Poon, W. W., & Blurton-Jones, M. M. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0336-1 · Cited by 54
Patel, D., Zhang, X., Farrell, J. J., Chung, J., Stein, T. D., Lunetta, K. L., & Farrer, L. A. (2021) · Translational Psychiatry · doi:10.1038/s41398-021-01373-z · Cited by 51
APOE ε4 genotype-dependent cerebrospinal fluid proteomic signatures in Alzheimer’s disease
Konijnenberg, E., Tijms, B. M., Gobom, J., Dobričić, V., Bos, I., Vos, S. J. B., Tsolaki, M., Verhey, F. R. J., Popp, J., Martínez‐Lage, P., et al. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00628-z · Cited by 50
Michaud, J.-P., Richard, K. L., & Rivest, S. (2011) · Molecular Neurodegeneration · doi:10.1186/1750-1326-6-5 · Cited by 48
Genetics of Gene Expression in the Aging Human Brain Reveal TDP-43 Proteinopathy Pathophysiology
Yang, H.-S., White, C. C., Klein, H.-U., Yu, L., Gaiteri, C., Ma, Y., Felsky, D., Mostafavi, S., Petyuk, V. A., Sperling, R. A., et al. (2020) · Neuron · doi:10.1016/j.neuron.2020.05.010 · Cited by 47
Pons, V., Lévesque, P., Plante, M.-M., & Rivest, S. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00747-7 · Cited by 46
Britschgi, M., Takeda-Uchimura, Y., Rockenstein, E., Johns, H., Masliah, E., & Wyss-Coray, T. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-220 · Cited by 45
Harnessing Immunoproteostasis to Treat Neurodegenerative Disorders
Golde, T. E. (2019) · Neuron · doi:10.1016/j.neuron.2019.02.027 · Cited by 45
IFN‐γ promotes τ phosphorylation without affecting mature tangles
Li, A., Ceballos‐Diaz, C., DiNunno, N., Levites, Y., Cruz, P. E., Lewis, J., Golde, T. E., & Chakrabarty, P. (2015) · The FASEB Journal · doi:10.1096/fj.15-275834 · Cited by 43
Self-citationTremblay, M.-È. (2021) · Brain, Behavior, & Immunity - Health · doi:10.1016/j.bbih.2021.100301 · Cited by 42
Rothman, S. M., Tanis, K. Q., Gandhi, P., Malkov, V. A., Marcus, J., Pearson, M. S., Stevens, R. C., Gilliland, J., Ware, C. M., Mahadomrongkul, V., et al. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1265-7 · Cited by 41
Improving preclinical to clinical translation in Alzheimer's disease research
Rizzo, S. J. S., Masters, A. R., Onos, K. D., Quinney, S. K., Sasner, M., Oblak, A. L., Lamb, B. T., & Territo, P. R. (2020) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12038 · Cited by 41
Dark microglia: Why are they dark?
Bisht, K., Sharma, K. P., Lacoste, B., & Tremblay, M. (2016) · Communicative & Integrative Biology · doi:10.1080/19420889.2016.1230575 · Cited by 39
Diabetic phenotype in mouse and humans reduces the number of microglia around β-amyloid plaques
Natunen, T., Martiskainen, H., Marttinen, M., Gabbouj, S., Koivisto, H., Kemppainen, S., Kaipainen, S., Takalo, M., Svobodová, H., Leppänen, L., et al. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00415-2 · Cited by 36
Rivera-Escalera, F., Matousek, S. B., Ghosh, S., Olschowka, J. A., & O’Banion, M. K. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2014.05.018 · Cited by 34
Walker, D. G. (2020) · Neuroimmunology and Neuroinflammation · doi:10.20517/2347-8659.2020.09 · Cited by 34
Network Analysis of a Membrane-Enriched Brain Proteome across Stages of Alzheimer’s Disease
Higginbotham, L., Dammer, E., Duong, D., Modeste, E., Montine, T., Lah, J., Levey, A., & Seyfried, N. (2019) · Proteomes · doi:10.3390/proteomes7030030 · Cited by 32
Microglia show differential transcriptomic response to Aβ peptide aggregates ex vivo and in vivo
McFarland, K. N., Ceballos, C., Rosario, A. M., Ladd, T. B., Moore, B. D., Golde, G., Wang, X., Allen, M., Ertekin‐Taner, N., Funk, C. C., et al. (2021) · Life Science Alliance · doi:10.26508/lsa.202101108 · Cited by 31
Self-citationKatsumata, Y., Nelson, P. T., Estus, S., & Fardo, D. W. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.10.017 · Cited by 30
A Therapeutic Strategy for Alzheimer's Disease Focused on Immune-inflammatory Modulation
Kim, S. H., Noh, M., Kim, H.-J., Oh, K., Park, J., Lee, S.-G., Moon, Y., Kim, Y.-E., Bae, J. S., Jin, H. K., et al. (2019) · Dementia and Neurocognitive Disorders · doi:10.12779/dnd.2019.18.2.33 · Cited by 30
Peng, S., Zeng, L., Haure‐Mirande, J., Wang, M., Huffman, D. M., Haroutunian, V. H., Ehrlich, M. E., Zhang, B., & Tu, Z. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.711524 · Cited by 29
A Brief Synopsis on the Genetics of Alzheimer’s Disease
Kamboh, M. I. (2018) · Current Genetic Medicine Reports · doi:10.1007/s40142-018-0155-8 · Cited by 26
Bemiller, S. M., Maphis, N. M., Formica, S. V., Wilson, G. N., Miller, C. M., Xu, G., Kokiko-Cochran, O. N., Kim, K.-W., Jung, S., Cannon, J. L., et al. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1310-6 · Cited by 24
Tato, C. M., Joyce-Shaikh, B., Banerjee, A., Chen, Y., Sathe, M., Ewald, S. E., Liu, M.-R., Gorman, D. M., McClanahan, T. K., Phillips, J. H., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0031680 · Cited by 23
Naproxen for presymptomatic Alzheimer disease
Hershey, L. A., & Lipton, R. B. (2019) · Neurology · doi:10.1212/wnl.0000000000007233 · Cited by 20
Zhu, K., Pieber, M., Han, J., Blomgren, K., Zhang, X., Harris, R. A., & Lund, H. (2020) · Glia · doi:10.1002/glia.23794 · Cited by 16
Rueda‐Carrasco, J., & Hong, S. Y. (2020) · Trends in Neurosciences · doi:10.1016/j.tins.2020.08.002 · Cited by 8
Aisen, P. S., Schafer, K. A., Grundman, M., Pfeiffer, E., Sano, M., Davis, K. L., Farlow, M. R., Jin, S., Thomas, R. G., Thal, L. J., et al. (2003) · JAMA · doi:10.1001/jama.289.21.2819 · Cited by 5
Peng, S., Zeng, L., Haure-mirande, J.-V., Wang, M., Huffman, D. M., Haroutunian, V., Ehrlich, M. E., Zhang, B., & Tu, Z. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.06.01.446628 · Cited by 2
Flagged first, then by citations
Cited by
Sorted by citations
Qin, J., Ma, Z., Chen, X., & Shu, S. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1103416 · Cited by 243
Khan, A. A., Mahendran, R. K., Perumal, K., & Faheem, M. (2024) · IEEE Transactions on Neural Systems and Rehabilitation Engineering · doi:10.1109/tnsre.2024.3357723 · Cited by 119
Therapeutic Potential of Allicin and Aged Garlic Extract in Alzheimer’s Disease
Tedeschi, P., Nigro, M., Travagli, A., Catani, M., Cavazzini, A., Merighi, S., & Gessi, S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23136950 · Cited by 61
Dysfunctional microglia and tau pathology in Alzheimer’s disease
Ayyubova, G. (2022) · Reviews in the Neurosciences · doi:10.1515/revneuro-2022-0087 · Cited by 36
New Insights into Microglial Mechanisms of Memory Impairment in Alzheimer’s Disease
Li, N., Deng, M., Hu, G., Li, N., Yuan, H., & Zhou, Y. (2022) · Biomolecules · doi:10.3390/biom12111722 · Cited by 30
Metadata
- Authors
- McFarland, K. N., & Chakrabarty, P.
- Affiliations
- University of Florida (US)
- Corresponding author
- Chakrabarty, Paramita
- Venue
- Neurotherapeutics
- Publisher
- Elsevier BV
- Published
- 2022-01
- Volume
- 19
- Issue
- 1
- Pages
- 186-208
- ISSN
- 1878-7479 (ISSN-L)
- PMC
- PMC9130399
- OpenAlex
- W4221004276
- Cited by
- 48
- References
- 265
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 15 · 2023: 10 · 2022: 7
- FWCI
- 1.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neurotherapeutics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- national institutes of health (P30AG066506, RF1AG064914)
- 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
- microglia, Alzheimer's disease, microglial activation, neuroinflammation, amyloid-beta, neurodegeneration, healthy aging, microglial phenotype, disease-modifying therapy
- MeSH terms
- Alzheimer Disease, Brain, Homeostasis, Humans, Neurons, Microglia
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
