The role of the immune system in neurodegenerative disorders: Adaptive or maladaptive?
Open accessAbstract
Neurodegenerative diseases share common features, including catastrophic neuronal loss that leads to cognitive or motor dysfunction. Neuronal injury occurs in an inflammatory milieu that is populated by resident and sometimes, infiltrating, immune cells - all of which participate in a complex interplay between secreted inflammatory modulators and activated immune cell surface receptors. The importance of these immunomodulators is highlighted by the number of immune factors that have been associated with increased risk of neurodegeneration in recent genome-wide association studies. One of the more difficult tasks for designing therapeutic strategies for immune modulation against neurodegenerative diseases is teasing apart beneficial from harmful signals. In this regard, learning more about the immune components of these diseases has yielded common themes. These unifying concepts should eventually enable immune-based therapeutics for treatment of Alzheimer׳s and Parkinson׳s diseases and amyotrophic lateral sclerosis. Targeted immune modulation should be possible to temper maladaptive factors, enabling beneficial immune responses in the context of neurodegenerative diseases. This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.
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In Alzheimer disease models, M1 functions promote removal of amyloid plaques, while M2 functions may facilitate amyloid spreading.
“In models of AD, M1 functions promote removal of amyloid plaques, while M2 functions may facilitate amyloid spreading (187).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [187]
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Microglia Function in the Central Nervous System During Health and Neurodegeneration
Colonna, M., & Butovsky, O. (2017) · Annual Review of Immunology · doi:10.1146/annurev-immunol-051116-052358 · Cited by 2,894 · see citing works
Microglia in physiology and disease
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Neuron-glia signaling in synapse elimination
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- Authors
- Doty, K. R., Guillot-Sestier, M.-V., & Town, T.
- Affiliations
- University of Southern California (US)
- Corresponding author
- Town, Terrence
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 1617
- Pages
- 155-173
- ISSN
- 0006-8993 (ISSN-L)
- PMC
- PMC4362937
- OpenAlex
- W2085480745
- Cited by
- 104
- References
- 238
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 12 · 2023: 10 · 2022: 9 · 2021: 11 · 2020: 8 · 2019: 6 · 2018: 6 · 2017: 13 · 2016: 10 · 2015: 4 · 2014: 1
- FWCI
- 0.75
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (5R00AG029726-04, 3R00AG029726-04S1)
- National Institute on Neurologic Disorders and Stroke (1R01NS076794-01)
- Alzheimer׳s Association Zenith Fellows Award (ZEN-10-174633)
- American Federation of Aging Research/Ellison Medical Foundation Julie Martin Mid-Career Award in Aging Research (M11472)
- Zilkha Neurogenetic Institute
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- neurodegenerative diseases, neuroinflammation, immune system, adaptive immunity, immunomodulation, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, neuronal loss
- MeSH terms
- Alzheimer Disease, Amyotrophic Lateral Sclerosis, Animals, Astrocytes, Brain, Encephalitis, Humans, Neurons, Parkinson Disease, Risk Factors, Microglia, Inflammation Mediators, Neurodegenerative Diseases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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