The DOI matches its Crossref record; 218 of the 220 references it cites were found in a registry or an index.
Immune attack: the role of inflammation in Alzheimer disease
Abstract
The past two decades of research into the pathogenesis of Alzheimer disease (AD) have been driven largely by the amyloid hypothesis; the neuroinflammation that is associated with AD has been assumed to be merely a response to pathophysiological events. However, new data from preclinical and clinical studies have established that immune system-mediated actions in fact contribute to and drive AD pathogenesis. These insights have suggested both novel and well-defined potential therapeutic targets for AD, including microglia and several cytokines. In addition, as inflammation in AD primarily concerns the innate immune system - unlike in 'typical' neuroinflammatory diseases such as multiple sclerosis and encephalitides - the concept of neuroinflammation in AD may need refinement.
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In the citing paper
“In brain tissue from human AD patients, microglia display the morphology (Heppner et al., 2015) and gene expression profile (Gjoneska et al., 2015; Mathys et al., 2019) characteristic of an activated cell state and cluster around β-amyloid plaques.”
From A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation (2023) · cites this paper as Heppner et al., 2015
In the citing paper
“Immune molecules like IL-1β, IL-6 and CCL2 are produced by brain endothelial cells against Aβ plaque [18].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [18]
In the citing paper
“glial activation is an indication of pro-inflammatory changes that is commonly found in AD brains”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [98]
In the citing paper
“In AD brains, microglia surrounding amyloid plaques display activated amoeboid morphologies with enlarged soma and retracted processes, indicating microglial response to protein accumulation or increased inflammatory mediators [41, 46-48].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [48]
In the citing paper
“indicating microglial response to protein accumulation or increased inflammatory mediators [41, 46-48].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [48]
Citations
Cites
1 retracted
Larson, M. E., Sherman, M. A., Amar, F., Nuvolone, M., Schneider, J. A., Bennett, D. A., Aguzzi, A., & Lesné, S. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.1858-12.2012 · Cited by 290
RetractedThe Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Mosmann, T. R., Cherwinski, H. M., Bond, M. W., Giedlin, M. A., & Coffman, R. L. (1986) · The Journal of Immunology · doi:10.4049/jimmunol.136.7.2348 · Cited by 7,553
Macrophage activation and polarization: nomenclature and experimental guidelines
Murray, P. J., Allen, J. E., Biswas, S. K., Fisher, E. A., Gilroy, D. W., Goerdt, S., Gordon, S., Hamilton, J. A., Ivashkiv, L. B., Lawrence, T., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.06.008 · Cited by 6,337
Astrocytes: Biology and pathology
Sofroniew, M. V., & Vinters, H. V. (2010) · Acta Neuropathologica · doi:10.1007/s00401-009-0619-8 · Cited by 5,196
Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide
Haass, C., & Selkoe, D. J. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2101 · Cited by 4,744
The M1 and M2 paradigm of macrophage activation: Time for reassessment
Martinez, F. O., & Gordon, S. (2014) · F1000Prime Reports · doi:10.12703/p6-13 · Cited by 4,689
Querfurth, H. W., & LaFerla, F. M. (2010) · New England Journal of Medicine · doi:10.1056/nejmra0909142 · Cited by 4,569
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
Synaptic Pruning by Microglia Is Necessary for Normal Brain Development
Paolicelli, R. C., Bolasco, G., Pagani, F., Maggi, L., Scianni, M., Panzanelli, P., Giustetto, M., Ferreira, T. A., Guiducci, E., Dumas, L., et al. (2011) · Science · doi:10.1126/science.1202529 · Cited by 4,244
Cited by
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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
Weinstein, G., Preis, S. R., Beiser, A. S., Kaess, B., Chen, T. C., Satizabal, C., Rahman, F., Benjamin, E. J., Vasan, R. S., & Seshadri, S. (2017) · Current Alzheimer Research · doi:10.2174/1567205014666170203094520 · Cited by 17
Liu, J., Lin, Y., Yang, Y., Guo, Y., Shang, Y., Zhou, B., Liu, T., Fan, J., & Wei, C. (2022) · Biochemical Pharmacology · doi:10.1016/j.bcp.2022.115149 · Cited by 12
Metadata
- Authors
- Heppner, F. L., Ransohoff, R. M., & Becher, B.
- Affiliations
- NeuroCure Cluster of Excellence (DE)
- Biogen (United States) (US)
- University of Zurich (CH)
- Corresponding author
- Heppner, Frank L.
- Ransohoff, Richard M.
- Becher, Burkhard
- Venue
- Nature Reviews Neuroscience
- Published
- 2015-05-20
- Volume
- 16
- Issue
- 6
- Pages
- 358-372
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- OpenAlex
- W1841850981
- Cited by
- 2,134
- References
- 220
- Citations by year
- 2026: 121 · 2025: 157 · 2024: 166 · 2023: 173 · 2022: 211 · 2021: 264 · 2020: 221 · 2019: 192 · 2018: 225 · 2017: 205 · 2016: 153 · 2015: 43
- FWCI
- 16.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- 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, innate immunity, microglia, cytokines, amyloid hypothesis, pathogenesis, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Humans, Inflammation
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