The DOI matches its Crossref record; 154 of the 156 references it cites were found in a registry or an index.
Danger-associated molecular patterns in Alzheimer’s disease
Open accessAbstract
Pathogen-associated molecular patterns (PAMPs) and endogenous “danger” signals, known as danger-associated molecular patterns (DAMPs), released from cells alert the innate immune system and activate several signal transduction pathways through interactions with the highly conserved pattern recognition receptors (PRRs). Both PAMPs and DAMPs directly induce proinflammatory cascades and trigger the formation of the inflammasome, mediating the release of cytokines. Here, we highlight the role of DAMPs, including amyloid β (Aβ), high-mobility group box 1 (HMGB1), the S100 family proteins, chromogranin A, and nucleic acids, in the innate-immune activation during the course of Alzheimer disease (AD), the most frequent neurodegenerative disorder.
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“In addition to aggregates, tissue injury also induces the extracellular release of DAMPs, such as mitochondrial DNA (mtDNA), high mobility group box 1 (HMGB1), S100 proteins, chromogranin A, adenosine 5′-triphosphate (ATP), and uric acid, from damaged brain cells. These DAMPs trigger neuroinflammation by activating pattern recognition receptors (PRRs), including TLRs, RAGE, NLRs, P2Y receptors”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [48]
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“In AD, Aβ can act as DAMP and its interaction with microglia creates an oxidative and neuroinflammatory environment through an increased production of ROS and release of proinflammatory cytokines [107].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [107]
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“PRRs bind to different species of Aβ with various affinities (71).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [71]
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1 retracted
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Metadata
- Authors
- Venegas, C., & Heneka, M. T.
- Affiliations
- University of Bonn (DE)
- Corresponding author
- Heneka, Michael T
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-10-21
- Volume
- 101
- Issue
- 1
- Pages
- 87-98
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- OpenAlex
- W2534771646
- Cited by
- 236
- References
- 156
- Citations by year
- 2026: 24 · 2025: 26 · 2024: 29 · 2023: 25 · 2022: 29 · 2021: 30 · 2020: 30 · 2019: 15 · 2018: 15 · 2017: 11
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- PubMed (publishedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion)
- DZNE Pub (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- damage-associated molecular patterns, Alzheimer's disease, innate immunity, pattern recognition receptors, pathogen-associated molecular patterns, inflammasome, amyloid-beta, HMGB1, S-100 protein, chromogranin A, nucleic acids, neuroinflammation, cytokine production
- MeSH terms
- Alarmins, Alzheimer Disease, Animals, Humans, Inflammation, Models, Biological, Receptors, Pattern Recognition, Molecular Targeted Therapy
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