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Role of Chemokines in the Development and Progression of Alzheimer’s Disease
Open accessAbstract
Alzheimer’s disease (AD) is a progressive neurogenerative disorder manifested by gradual memory loss and cognitive decline due to profound damage of cholinergic neurons. The neuropathological hallmarks of AD are intracellular deposits of neurofibrillary tangles (NFTs) and extracellular aggregates of amyloid β (Aβ). Mounting evidence indicates that intensified neuroinflammatory processes play a pivotal role in the pathogenesis of AD. Chemokines serve as signaling molecules in immune cells but also in nerve cells. Under normal conditions, neuroinflammation plays a neuroprotective role against various harmful factors. However, overexpression of chemokines initiates disruption of the integrity of the blood–brain barrier, facilitating immune cells infiltration into the brain. Then activated adjacent glial cells–astrocytes and microglia, release massive amounts of chemokines. Prolonged inflammation loses its protective role and drives an increase in Aβ production and aggregation, impairment of its clearance, or enhancement of tau hyperphosphorylation, contributing to neuronal loss and exacerbation of AD. Moreover, chemokines can be further released in response to growing deposits of toxic forms of Aβ. On the other hand, chemokines seem to exert multidimensional effects on brain functioning, including regulation of neurogenesis and synaptic plasticity in regions responsible for memory and cognitive abilities. Therefore, underexpression or complete genetic ablation of some chemokines can worsen the course of AD. This review covers the current state of knowledge on the role of particular chemokines and their receptors in the development and progression of AD. Special emphasis is given to their impact on forming Aβ and NFTs in humans and in transgenic murine models of AD.
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“consistent with the known capacity of CCL2 to break down the blood brain barrier and recruit peripheral immune cells to sites of damage.58–62”
From TET2-mutant myeloid cells mitigate Alzheimer’s disease progression via CNS infiltration and enhanced phagocytosis in mice (2025) · cites this paper as [60]
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“Within the brain, chemokines may be released by neurons, astrocytes or microglia and contribute to neurogenesis, synaptic plasticity and also to neuroinflammation (Wojcieszak et al., 2022).”
BackgroundImmune response of BV-2 microglial cells is impacted by peroxisomal beta-oxidation
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“These chemokines are small cytokines that play a key role in the regulation of immune cell migration and actively participate in neurodegenerative processes (Wojcieszak et al., 2022).”
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“Furthermore, the chemokine network forms a positive feedback loop with A β and tau protein pathology: A β oligomers stimulate microglia to release CCL3 and CCL5, which in turn exacerbate the hyperphosphorylation of tau protein within neurons (Jorda et al., 2020; Wojcieszak et al., 2022).”
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“CXCL12 primarily signals through its receptors CXCR4 and, in the adult brain, it modulates neurotransmission, enhances synaptic plasticity, and generally provides neuroprotective effects against various insults [50].”
CXCL10 contributes to female-specific pathological progression in tauopathy model mice
Uenishi, R., Kawata, R., Manabe, T., Matsuba, Y., Mihira, N., Takeo, T., Saido, T. C., Hijioka, M., & Saito, T. (2026) · Journal of Neuroinflammation · doi:10.1186/s12974-026-03989-8 · Cited by 1
“While altered chemokine levels have been reported in the cerebrospinal fluid (CSF) and brain tissues of patients with AD [14], the specific molecular mediators linking glial-derived chemokine signaling to T cell infiltration and tau pathology—especially in a sex-dependent manner—remain largely…”
Sura, S., Jagadeesan, S., Moklas, M. A. M., Masrudin, S. S., Dandala, K. C. R., Judson, J. P., & Nor, N. H. M. (2026) · Molecular Biology Reports · doi:10.1007/s11033-026-12578-0 · Cited by 2
Nguyen, H. D., Jo, W. H., Cha, J. O., Hoang, N. M. H., & Kim, M.-S. (2024) · Toxicological Research · doi:10.1007/s43188-024-00228-1 · Cited by 1
Juvenal, G. D. A., Meinerz, C., Ayupe, A. C., Campos, H. C., Reis, E. M. R., Longo, B. M., Pillat, M. M., & Ulrich, H. (2024) · Cell & Bioscience · doi:10.1186/s13578-024-01251-3 · Cited by 1
“The chemokines CCL2, CCL3, CCL4, CCL5, CXCL10, and CXCL5 and the chemokine receptor CX3CR1 orchestrate neuroinflammation by attracting and activating microglia and play an important role in cell-to-cell communication in the CNS [31].”
BackgroundRico, E. M. G., Joseph, P., Noutsos, C., & Poon, K. (2024) · Neuroscience · doi:10.1016/j.neuroscience.2024.07.007 · Cited by 1
Wojcieszak, J. (2023) · Farmacja Polska · doi:10.32383/farmpol/166243 · Cited by 1
Self-citationNAD+ hydrolase Sarm1 is a key driver of synapse degeneration and memory loss in Alzheimer’s disease
Fan, F., Joshi, P., Liu, X., Kotturu, S. K., Abiola, M., Liu, Q., & Lou, X. (2025) · doi:10.64898/2025.12.21.695860
SARS-CoV-2 neurotropism-induced anxiety/depression-like behaviors require Microglia activationPreprint
Ge, Q., Zhou, S., Porras, J., Fu, P., Wang, T., Du, J., & Li, K. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.02.560570 · Cited by 1
“…studies support the idea that elevated cytokines like IL-1β, IL-6, CCL2 and TNF-α associated with the development of anxiety and depression-like behaviors in mice (65-68), underscoring the contribution of neuroinflammation to the behavioral manifestations observed following SARS-CoV-2 infection.”
BackgroundWang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208974
Wang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208992
Wang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208983
Wang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208980
Wang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208971
Wang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208977
Wang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208989
Early cognitive dysfunction development immunological predictors in the ischemic stroke acute period
Tynterova, A. M. (2024) · Russian neurological Journal · doi:10.30629/2658-7947-2024-29-2-24-33
Catalão, C. H. R., Beeghly, C., Iwunze, N., Barichello, T., & Giridharan, V. V. (2025) · Neuromethods · doi:10.1007/978-1-0716-4474-4_17
Huang, L., Liu, Q., Ma, Z., Xue, J., Tian, X., Zhao, X., Zheng, Y., Wei, X., Yu, X., Feng, Y., et al. (2025) · Food Science and Human Wellness · doi:10.26599/fshw.2025.9250594
Changes of Microglial Cells in the Progression of Neurodegeneration in Natural Prion Disease
Monzón, M., Pérez, J. S., Hernández, R. S., Sarasa, R., Garcés, M., Bartolomé, M. J. L., & Badiola, J. J. (2025) · Frontiers in Bioscience-Landmark · doi:10.31083/fbl47074
“Thus, the modulation of these chemokines could also represent therapeutic strategies against neurodegeneration [43].”
Glial Cells, Cytokines, and Inflammasomes in Neurodegeneration
Patil, V. S., Desai, A., & Meena, H. (2025) · Springer eBooks · doi:10.1007/978-981-95-3945-1_3
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711651
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711621
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711639
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711654
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711624
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711672
Wang, P., Anderson, D. E., & Ye, Y. (2023) · Figshare · doi:10.6084/m9.figshare.24208986
Juvenal, G. D. A., Meinerz, C., Ayupe, A. C., Campos, H. C., Reis, E. M., Longo, B. M., Pillat, M. M., & Ulrich, H. (2024) · Figshare · doi:10.6084/m9.figshare.26061505
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711636
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711642
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711657
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van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711663
Juvenal, G. D. A., Meinerz, C., Ayupe, A. C., Campos, H. C., Reis, E. M., Longo, B. M., Pillat, M. M., & Ulrich, H. (2024) · Figshare · doi:10.6084/m9.figshare.26735739
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711630
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26711648
Juvenal, G. D. A., Meinerz, C., Ayupe, A. C., Campos, H. C., Reis, E. M., Longo, B. M., Pillat, M. M., & Ulrich, H. (2024) · Figshare · doi:10.6084/m9.figshare.26735730
van Olst, L., Kamermans, A., Halters, S., van der Pol, S. M. A., Rodríguez, E., Verberk, I. M. W., Verberk, S. G. S., Wessels, D. W. R., Rodriguez-Mogeda, C., Verhoeff, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25687615
Juvenal, G. D. A., Meinerz, C., Ayupe, A. C., Campos, H. C., Reis, E. M., Longo, B. M., Pillat, M. M., & Ulrich, H. (2024) · Figshare · doi:10.6084/m9.figshare.26735724
Metadata
- Authors
- Wojcieszak, J., Kuczyńska, K., & Zawilska, J. B.
- Affiliations
- Karolinska Institutet (SE)
- Medical University of Lodz (PL)
- Corresponding author
- Zawilska, Jolanta B.
- Venue
- Journal of Molecular Neuroscience
- Published
- 2022-07-12
- Volume
- 72
- Issue
- 9
- Pages
- 1929-1951
- ISSN
- 0895-8696 (ISSN-L)
- 1559-1166
- PMC
- PMC9392685
- OpenAlex
- W4285089500
- Cited by
- 97
- References
- 146
- Citations by year
- 2026: 25 · 2025: 20 · 2024: 35 · 2023: 17
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Journal of Molecular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Uniwersytet Łódzki (503-31-001)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, chemokines, chemokine receptors, neuroinflammation, amyloid-beta, neurofibrillary tangles, blood-brain barrier, microglia, astrocytes, tau hyperphosphorylation, neurogenesis, synaptic plasticity, cholinergic neurons, transgenic mouse model
- MeSH terms
- Alzheimer Disease, Animals, Humans, Amyloid beta-Peptides, Neurofibrillary Tangles, Microglia, Chemokines, Mice
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