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 the citing paper
“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]
In the citing paper
“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
Yang, H., Lundbäck, P., Ottosson, L., Erlandsson-Harris, H., Venereau, E., Bianchi, M. E., Al-Abed, Y., Andersson, U., Tracey, K. J., & Antoine, D. J. (2012) · Molecular Medicine · doi:10.2119/molmed.2011.00389 · Cited by 407
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
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Alzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484
Mitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases
Lin, M. T., & Beal, M. F. (2006) · Nature · doi:10.1038/nature05292 · Cited by 6,455
Neuroinflammation in Alzheimer's disease
Heneka, M. T., Carson, M. J., Khoury, J. E., Landreth, G. E., Brosseron, F., Feinstein, D. L., Jacobs, A. H., Wyss-Coray, T., Vitorica, J., Ransohoff, R. M., et al. (2015) · The Lancet Neurology · doi:10.1016/s1474-4422(15)70016-5 · Cited by 6,226
Self-citationTolerance, Danger and the Extended Family
Matzinger, P. (1994) · Annual Review of Immunology · doi:10.1146/annurev.iy.12.040194.005015 · Cited by 5,107
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221
Circulating mitochondrial DAMPs cause inflammatory responses to injury
Zhang, Q., Raoof, M., Chen, Y., Sumi, Y., Sursal, T., Junger, W., Brohi, K., Itagaki, K., & Hauser, C. J. (2010) · Nature · doi:10.1038/nature08780 · Cited by 3,812
Toll-like receptors in innate immunity
Takeda, K. (2004) · International Immunology · doi:10.1093/intimm/dxh186 · Cited by 3,328
Research works printed but not linked: 2
- Wyss-Coray, 2006, Inflammation in Alzheimer disease: driving force, bystander or beneficial response, Nat. Med., 12, 1005
- Scholtzova, 2014, Amyloid β and tau Alzheimer’s disease related pathology is reduced by Toll-like receptor 9 stimulation, Acta Neuropathol. Commun., 2, 101
Cited by
Sorted by citations
Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?
Leng, F., & Edison, P. (2021) · Nature Reviews Neurology · doi:10.1038/s41582-020-00435-y · Cited by 3,179
Role of neuroinflammation in neurodegeneration development
Zhang, W., Xiao, D., Mao, Q., & Xia, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01486-5 · Cited by 1,668
“These DAMPs trigger neuroinflammation by activating pattern recognition receptors (PRRs), including TLRs, RAGE, NLRs, P2Y receptors among others, which are expressed either on the surface of cerebral myeloid cells or intracellularly.(48) In summary, it has been clear that the pathogenic protein aggregation and neuroin…”
BackgroundDamage-associated molecular patterns in inflammatory diseases
Roh, J. S., & Sohn, D. H. (2018) · Immune Network · doi:10.4110/in.2018.18.e27 · Cited by 1,261
Microglia in Alzheimer's disease
Sarlus, H., & Heneka, M. T. (2017) · Journal of Clinical Investigation · doi:10.1172/jci90606 · Cited by 911
Self-citationMicroglia in Neurological Diseases: A Road Map to Brain-Disease Dependent-Inflammatory Response
Bachiller, S., Jiménez-Ferrer, I., Paulus, A., Yang, Y., Swanberg, M., Deierborg, T., & Boza‐Serrano, A. (2018) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2018.00488 · Cited by 750
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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