Complement in the pathogenesis of Alzheimer’s disease
Open accessAbstract
The emergence of complement as an important player in normal brain development and pathological remodelling has come as a major surprise to most scientists working in neuroscience and almost all those working in complement. That a system, evolved to protect the host against infection, should have these unanticipated roles has forced a rethink about what complement might be doing in the brain in health and disease, where it is coming from, and whether we can, or indeed should, manipulate complement in the brain to improve function or restore homeostasis. Complement has been implicated in diverse neurological and neuropsychiatric diseases well reviewed elsewhere, from depression through epilepsy to demyelination and dementia, in most complement drives inflammation to exacerbate the disease. Here, I will focus on just one disease, the most common cause of dementia, Alzheimer's disease. I will briefly review the current understanding of what complement does in the normal brain, noting, in particular, the many gaps in understanding, then describe how complement may influence the genesis and progression of pathology in Alzheimer's disease. Finally, I will discuss the problems and pitfalls of therapeutic inhibition of complement in the Alzheimer brain.
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Recently, a number of novel agents targeting the complement system are being developed and tested in clinical trials for potential effective therapy for AD.
“Recently, a number of novel agents targeting the complement system are being developed and tested in clinical trials for potential effective therapy for AD [97].”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [97]
The “Targeting complement in AD” section describes C1q-blocking antibodies developed for AD and other anti-complement drugs in development. It does not say these agents are being tested in AD clinical trials; the Concluding remarks instead call such trials urgently needed and refer to future trials. (LLM, conf=0.88)
Experimental — accuracy not yet measuredStrong evidence has implicated the complement system in the pathogenesis of Alzheimer's disease.
“Strong evidence has implicated the complement system in the pathogenesis of Alzheimer’s disease [72–76]”
Inappropriate control of the classical complement cascade causes unresolvable inflammation and disease.
“Inappropriate control of the classical complement cascade causes unresolvable inflammation and disease (Hong et al. , 2016; Hansen, Hanson and Sheng, 2018; Morgan, 2018).”
From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as Morgan, 2018
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Synaptic Pruning in Alzheimer’s Disease: Role of the Complement System
Brucato, F. H., & Benjamin, D. E. (2020) · Global Journal of Medical Research · doi:10.34257/gjmrfvol20is6pg1 · Cited by 22 · see citing works
Zarantonello, A., Présumey, J., Simoni, L., Yalçın, E., Fox, R. G., Hansen, A. G., Olesen, H. G., Thiel, S., Johnson, M. B., Stevens, B., et al. (2020) · The Journal of Immunology · doi:10.4049/jimmunol.2000528 · Cited by 23 · see citing works
Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease
Shadid, A., Hok, K. D., Domozhirov, A. Y., Mills, T., Doursout, M. F., Banda, N. K., Restrepo, M. I., & Shivshankar, P. (2025) · Immune Network · doi:10.4110/in.2025.25.e32 · Cited by 22 · see citing works
Espericueta, V., Manughian-Peter, A. O., Bally, I., Thielens, N. M., & Fraser, D. A. (2019) · Molecular Immunology · doi:10.1016/j.molimm.2019.10.008 · Cited by 22 · see citing works
Neuroglia Cells Transcriptomic in Brain Development, Aging and Neurodegenerative Diseases
Pinosanu, L. R., Căpitănescu, B., Glăvan, D., Godeanu, S., Fernández‐Cadenas, I., Doeppner, T. R., Hermann, D. M., Bălşeanu, T. A., Cătălin, B., & Popa‐Wagner, A. (2022) · Aging and Disease · doi:10.14336/ad.2022.0621 · Cited by 22 · see citing works
The Role of Complement C3a Receptor in Stroke
Ahmad, S., Bhatia, K., Kindelin, A., & Ducruet, A. F. (2019) · NeuroMolecular Medicine · doi:10.1007/s12017-019-08545-7 · Cited by 21 · see citing works
Beneficial versus Detrimental Effects of Complement–Microglial Interactions in Alzheimer’s Disease
Ayyubova, G., & Fazal, N. (2024) · Brain Sciences · doi:10.3390/brainsci14050434 · Cited by 20 · see citing works
Human Plasma Protein Corona of Aβ Amyloid and Its Impact on IAPP Cross-Seeding
Nandakumar, A., Xing, Y., Aranha, R., Faridi, A., Kakinen, A., Javed, I., Koppel, K., Pilkington, E. H., Purcell, A., Davis, T., et al. (2020) · Biomacromolecules · doi:10.1021/acs.biomac.9b01650 · Cited by 20 · see citing works
Tajmim, A., Cuevas-Ocampo, A. K., Siddique, A. B., Qusa, M. H., King, J. A., Abdelwahed, K. S., Sonju, J. J., & Sayed, K. A. E. (2021) · Nutrients · doi:10.3390/nu13051702 · Cited by 19 · see citing works
Vidal, C., & Li, Z. (2021) · Cells · doi:10.3390/cells10030546 · Cited by 19 · see citing works
Pomilio, A. B., Vitale, A. A., & Lazarowski, A. (2022) · Current Medicinal Chemistry · doi:10.2174/0929867329666221003101548 · Cited by 18 · see citing works
Temporal and Sex-Linked Protein Expression Dynamics in a Familial Model of Alzheimer’s Disease
Lopes, F. B. T. P., Schlatzer, D., Wang, R., Li, X., Feng, E., Koyutürk, M., Qi, X., & Chance, M. R. (2022) · Molecular & Cellular Proteomics · doi:10.1016/j.mcpro.2022.100280 · Cited by 16 · see citing works
Association between APOE genotype and microglial cell morphology
Kloske, C. M., Gearon, M. D., Weekman, E. M., Rogers, C. B., Patel, E., Bachstetter, A. D., Nelson, P. T., & Wilcock, D. M. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlad031 · Cited by 17 · see citing works
- Authors
- Morgan, B. P.
- Affiliations
- Cardiff University (GB)
- Corresponding author
- Morgan, B. Paul
- ORCID
- Morgan, B. Paul
- Venue
- Seminars in Immunopathology
- Published
- 2017-11-13
- Volume
- 40
- Issue
- 1
- Pages
- 113-124
- ISSN
- 1863-2297 (ISSN-L)
- 1863-2300
- PMC
- PMC5794825
- OpenAlex
- W2769984699
- Cited by
- 194
- References
- 93
- Citations by year
- 2026: 14 · 2025: 16 · 2024: 35 · 2023: 16 · 2022: 18 · 2021: 32 · 2020: 31 · 2019: 22 · 2018: 10
- FWCI
- 1.77
- Type
- journal article
- Language
- en
- Update notices
- correction (2018-09-21)
- Open access
- hybrid
- doi.org
- Locations
- Seminars in Immunopathology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
- Funders
- Cardiff University
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- complement system, Alzheimer's disease, complement inhibition therapy, neuroinflammation, brain homeostasis, dementia pathogenesis
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