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 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]
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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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