The DOI matches its Crossref record; 178 of the 178 references it cites were found in a registry or an index.
The identity and function of microglia in neurodegeneration
Abstract
The predominant type of immune cell in the brain is the microglia, a type of tissue-resident macrophage. In a variety of neurodegenerative settings, microglia alter their transcriptional profile, morphology and function in similar ways; thus, these activated cells have been called 'degeneration- or disease-associated microglia' (DAM). These activated microglia can perform different functions and exert both positive effects and negative effects in different mouse disease models. In humans, mutations in genes expressed in microglia are linked to various neurodegenerative diseases. Here we provide an overview of the common microglial response to neurodegeneration and key contributing pathways; delineate the multifaceted functions of activated microglia spanning various diseases; and discuss insights from the study of human disease-associated genes. We argue that strong evidence from both mouse models and human genetics causally links the function of activated microglia to neurodegeneration.
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In the citing paper
“The DAM phenotype has been proposed to represent a universal and intrinsic microglial response program to CNS disease, since it appears to be retained across a number of neurodegenerative and non-neurodegenerative diseases [74, 291]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [291]
In the citing paper
“DAM-expressed factors, such as apolipoprotein, colony-stimulating factor 1 (CSF1) and secreted phosphoprotein 1, act as autocrine ligands on DAM-expressed receptors, together sustaining and perpetuating the neurodegenerative phenotype [291]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [291]
In the citing paper
“complement activation, which is important for microglial phagocytosis, can exacerbate synaptic loss [152, 284, 291] and contribute to memory loss and cognitive decline [75]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [291]
In the citing paper
“Microglia are classified into two subtypes: classically activated (M1) cells, which secrete proinflammatory cytokines, and alternatively activated (M2) cells, which promote tissue regeneration and repair [9–12].”
From Neuron secrete exosomes containing miR-9-5p to promote polarization of M1 microglia in depression (2022) · cites this paper as [11]
In the citing paper
“Microgliosis is a known feature of AD [reviewed in (92, 93)]”
From The Transcriptional Landscape of Microglial Genes in Aging and Neurodegenerative Disease (2019) · cites this paper as [92]
Citations
Cites
1 retracted
Microglia-dependent synapse loss in type I interferon-mediated lupus
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Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
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Neurotoxic reactive astrocytes are induced by activated microglia
Liddelow, S. A., Guttenplan, K. A., Clarke, L. E., Bennett, F. C., Bohlen, C. J., Schirmer, L., Bennett, M. L., Münch, A. E., Chung, W.-S., Peterson, T. C., et al. (2017) · Nature · doi:10.1038/nature21029 · Cited by 7,971
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A Unique Microglia Type Associated with Restricting Development of Alzheimer’s Disease
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Self-citationFate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages
Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M. F., Conway, S. J., Ng, L. G., Stanley, E. R., et al. (2010) · Science · doi:10.1126/science.1194637 · Cited by 5,175
DeJesus-Hernandez, M., Mackenzie, I. R., Boeve, B. F., Boxer, A. L., Baker, M., Rutherford, N. J., Nicholson, A. M., Finch, N. A., Flynn, H., Adamson, J., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.011 · Cited by 4,936
A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD
Renton, A. E., Majounie, E., Waite, A., Simón-Sánchez, J., Rollinson, S., Gibbs, J. R., Schymick, J. C., Laaksovirta, H., van Swieten, J. C., Myllykangas, L., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.010 · Cited by 4,409
Meta-Analysis of 74,046 Individuals Identifies 11 New Susceptibility Loci for Alzheimer’s Disease
(EADI), E. A. D. I., Lambert, J.-C., (GERAD), G. A. E. R. I. A. D., Alzheimer's Disease Genetic Consortium (ADGC), (CHARGE), C. F. H. A. A. R. I. G. E., Ibrahim-Verbaas, C. A., Harold, D., Naj, A. C., Sims, R., Bellenguez, C., et al. (2013) · Nature Genetics · doi:10.1038/ng.2802 · Cited by 4,336
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Targeting microglia: A new strategy for the treatment of Alzheimer's disease
Zheng, M., Yang, M., Su, W., Tian, L., & Gao, W. (2026) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2026.578966
Díaz, D., Alonso, E. M. B., Pérez-Revuelta, L., Zapata-Acevedo, J. F., Torossian, F., Anginot, A., Alonso, J. R., Bousse‐Kerdilès, M. L., & Weruaga, E. (2026) · Journal of Tissue Engineering · doi:10.1177/20417314261442787
Diaz, V. C., Sunshine, M., Hu, F., Shah, S., Huang, W., Thompson, C. I., Wolin, M. S., Subbian, S., LaGamma, E. F., & Vinukonda, G. (2026) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2026.1812529
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Jaganathan, R., Vijayakumar, S., Chen, Y., Ye, J., Bakthavatchalam, P., Wankhar, D., Yang, C., Iyaswamy, A., & Li, M. (2026) · Neurobiology of Disease · doi:10.1016/j.nbd.2026.107555
Lajqi, T., Köstlin‐Gille, N., Birdir, C., Hebel, J., Miftari, I., Bauer, R., Zarogiannis, S. G., Funaya, C., Gille, C., & Dietz‐Ziegler, S. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1858954
The Neuroimmune Duality of CD4⁺ T Cells: Drivers of Damage and Repair in the Brain
Kumar, N., Mir, P. A., Bhutia, G. T., Uppal, J., Kaur, A., Kaur, G., & Gupta, S. K. (2026) · Molecular Neurobiology · doi:10.1007/s12035-026-06138-7
Toyoda, H. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27177597
Metadata
- Authors
- Song, W. M., & Colonna, M.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Colonna, Marco
- Venue
- Nature Immunology
- Published
- 2018-09-24
- Volume
- 19
- Issue
- 10
- Pages
- 1048-1058
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2891888347
- Semantic Scholar
- 56fd070c6693804f7ada07ce3ee33529dfa55dbf
- Cited by
- 308
- References
- 178
- Citations by year
- 2026: 21 · 2025: 28 · 2024: 37 · 2023: 49 · 2022: 53 · 2021: 42 · 2020: 42 · 2019: 33 · 2018: 3
- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Keywords
- microglia, neurodegeneration, disease-associated microglia, microglial activation, tissue-resident macrophages, microglial morphology, neurodegenerative disease models, microglial function
- MeSH terms
- Animals, Humans, Microglia, Neurodegenerative Diseases
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