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Innate Immunity and Neurodegeneration
Open accessAbstract
The innate immune system plays diverse roles in health and disease. It represents the first line of defense against infection and is involved in tissue repair, wound healing, and clearance of apoptotic cells and cellular debris. Excessive or nonresolving innate immune activation can lead to systemic or local inflammatory complications and cause or contribute to the development of inflammatory diseases. In the brain, microglia represent the key innate immune cells, which are involved in brain development, brain maturation, and homeostasis. Impaired microglial function, either through aberrant activation or decreased functionality, can occur during aging and during neurodegeneration, and the resulting inflammation is thought to contribute to neurodegenerative diseases. This review highlights recent advances in our understanding of the influence of innate immunity on neurodegenerative disorders such as Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease.
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“Aged glial cells respond less efficiently to antigens, including amyloid-β (Aβ) and α-synuclein, and have reduced phagocytic and antiinflammatory capacity (161–163).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [162]
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“Both receptors are expressed in immune cells, such as microglia, but also in neurons [3, 4, 7, 8].”
From Neurodegenerative disease-associated microRNAs acting as signaling molecules modulate CNS neuron structure and viability (2025) · cites this paper as [3]
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“Toll-like receptors (TLRs) contribute to such central nervous system (CNS) injury by triggering inflammation and cell-autonomous damage [3, 4].”
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Metadata
- Authors
- Labzin, L. I., Heneka, M. T., & Latz, E.
- Affiliations
- MRC Laboratory of Molecular Biology (GB)
- University of Massachusetts Chan Medical School (US)
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 2018-01-29
- Volume
- 69
- Issue
- 1
- Pages
- 437-449
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- OpenAlex
- W2735217968
- Cited by
- 319
- References
- 80
- Citations by year
- 2026: 11 · 2025: 30 · 2024: 37 · 2023: 35 · 2022: 42 · 2021: 53 · 2020: 53 · 2019: 32 · 2018: 26
- FWCI
- 2.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, other-oa)
- DZNE Pub (submittedVersion)
- Funders
- EU Joint Programme – Neurodegenerative Disease Research
- Deutsche Forschungsgemeinschaft (SFB1089, SPP-1923)
- National Institutes of Health
- National Health and Medical Research Council
- National Heart, Lung, and Blood Institute (R01HL112661)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- innate immunity, neurodegeneration, microglia, neuroinflammation, Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, Huntington's disease, microglial activation, brain homeostasis, aging
- MeSH terms
- Alzheimer Disease, Amyotrophic Lateral Sclerosis, Humans, Huntington Disease, Immunity, Innate, Inflammation, Parkinson Disease, Microglia, Neurodegenerative Diseases
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