The DOI matches its Crossref record; 149 of the 149 references it cites were found in a registry or an index.
Microglial priming of antigen presentation and adaptive stimulation in Alzheimer’s disease
Open accessAbstract
The prominent pathological consequences of Alzheimer's disease (AD) are the misfolding and mis-sorting of two cellular proteins, amyloid-β and microtubule-associated protein Tau. The accumulation of toxic phosphorylated Tau inside the neurons induces the increased processing of amyloid-β-associated signaling cascade and vice versa. Neuroinflammation-driven synaptic depletion and cognitive decline are substantiated by the cross talk of activated microglia and astroglia, leading to neuron degeneration. Microglia are the brain-resident immune effectors that prove their diverse functions in maintaining CNS homeostasis via collaboration with astrocytes and T lymphocytes. Age-related senescence and chronic inflammation activate microglia with increased pro-inflammatory markers, oxidative damage and phagocytosis. But the improper processing of misfolded protein via lysosomal pathway destines the spreading of 'seed' constituents to the nearby healthy neurons. Primed microglia process and present self-antigen such as amyloid-β and modified Tau to the infiltrated T lymphocytes through MHC I/II molecules. After an effective conversation with CD4 + T cells, microglial phenotype can be altered from pro-active M1 to neuro-protective M2 type, which corresponds to the tissue remodeling and homeostasis. In this review, we are focusing on the change in functionality of microglia from innate to adaptive immune response in the context of neuroprotection, which may help in the search of novel imm…
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“The recent finding therefore suggests that at least some plaque-associated microglia may borrow elements of lymphoid signaling logic rather than merely presenting antigen to lymphocytes [44,45,46].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [44]
In the citing paper
“Reviews of microglia–lymphocyte communication have emphasized that microglia may act as local regulators of lymphocyte activation, particularly when blood–brain barrier dysfunction or chronic neuroinflammation allows greater immune-cell trafficking into the CNS.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [44]
In the citing paper
“In inflammatory and neurodegenerative settings, microglia can upregulate antigen-presentation machinery, respond to interferon-γ and other lymphocyte-derived cytokines, and influence T-cell behavior within or near the central nervous system.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [44]
In the citing paper
“They can express molecules associated with antigen presentation, including MHC class II–related genes and co-stimulatory ligands such as CD80 or CD86, especially under inflammatory conditions.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [44]
Citations
Cites
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Neurotoxic reactive astrocytes are induced by activated microglia
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Neurodegenerative diseases and oxidative stress
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Microglia: Active sensor and versatile effector cells in the normal and pathologic brain
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Host microbiota constantly control maturation and function of microglia in the CNS
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Advanced glycation end-products: A review
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Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases
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Contributions of Age-Related Thymic Involution to Immunosenescence and Inflammaging
Thomas, R., Wang, W., & Su, D.-M. (2020) · Immunity & Ageing · doi:10.1186/s12979-020-0173-8 · Cited by 442
Challenges and hopes for Alzheimer’s disease
Tatulian, S. A. (2022) · Drug Discovery Today · doi:10.1016/j.drudis.2022.01.016 · Cited by 291
Xie, M., Liu, Y. U., Zhao, S., Zhang, L., Bosco, D. B., Pang, Y.-P., Zhong, J., Sheth, U., Martens, Y. A., Zhao, N., et al. (2022) · Nature Neuroscience · doi:10.1038/s41593-021-00975-6 · Cited by 157
Brahmi (Bacopa monnieri): An ayurvedic herb against the Alzheimer's disease
Dubey, T., & Chinnathambi, S. (2019) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2019.108153 · Cited by 151
Self-citationThe interaction between ageing and Alzheimer's disease: insights from the hallmarks of ageing
Liu, Y., Tan, Y., Zhang, Z., Yi, M., Zhu, L., & Peng, W. (2024) · Translational Neurodegeneration · doi:10.1186/s40035-024-00397-x · Cited by 156
Metadata
- Authors
- Das, R., & Chinnathambi, S.
- Affiliations
- National Chemical Laboratory (IN)
- Corresponding author
- Chinnathambi, Subashchandrabose
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2019-05-15
- Volume
- 76
- Issue
- 19
- Pages
- 3681-3694
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11105582
- OpenAlex
- W2945276138
- Cited by
- 147
- References
- 149
- Citations by year
- 2026: 18 · 2025: 28 · 2024: 24 · 2023: 22 · 2022: 8 · 2021: 29 · 2020: 16 · 2019: 1
- FWCI
- 1.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Department of Biotechnology , Ministry of Science and Technology (DBT-HDDB)- BT/PR/15780/MED/122/4/2016)
- Council of Scientific and Industrial Research (CSIR NCL MLP 029526)
- 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
- Alzheimer's disease, microglia, antigen presentation, neuroinflammation, amyloid-beta, tau protein, CD4+ T cells, M1/M2 microglial polarization, neuroprotection, astroglia, lysosomal processing, immunotherapy
- MeSH terms
- Alzheimer Disease, Brain, Humans, Immunotherapy, T-Lymphocytes, Neuroimmunomodulation, Protein Folding, Microglia, Antigen Presentation, Adaptive Immunity
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