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Microglial Activation and Chronic Neurodegeneration
Open accessAbstract
Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurodegenerative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-α, nitric oxide, interleukin-1β, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson's disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype.
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“MiRNAs can ameliorate degeneration by suppressing microglial activation in the brain and are therefore considered as a therapeutic approach for neurodegenerative diseases (Lull and Block 2010).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Lull and Block 2010
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“The notion that neuroinflammatory processes contribute to disease was once provocative, yet recent studies have uncovered multiple mechanisms by which aberrant gliosis causes detrimental neuroinflammation that can influence tau pathology and accelerate neurodegeneration.”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [6]
In the citing paper
“After this acute M1 activation, microglial cells can suffer an uncontrolled activation leading to a state of chronic inflammation. In this state, microglia release neurotoxic inflammatory factors (TNF-α, IL-1α, IL-1β, IL-6, NO, hydrogen peroxide, superoxide anion, chemokines, and glutamate), which lead to neuronal death (Block et al., 2007; Lull and Block, 2010; Burguillos et al., 2011; Kettenmann”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Lull and Block, 2010
In the citing paper
“Neuroinflammation is a characteristic of neurodegenerative diseases, including PD, in which microglia confer pathogenic and exacerbating effects (Lull and Block, 2010; Zhao et al., 2020).”
From Mechanism of miR-132-3p Promoting Neuroinflammation and Dopaminergic Neurodegeneration in Parkinson’s Disease (2022) · cites this paper as Lull and Block, 2010
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BackgroundMethodInfluentialA novel tauopathy model mimicking molecular and spatial aspects of human tau pathology
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Badell‐Grau, R. A., Pakravesh, K., Thai, K. E., Son, F., Chen, R., Rainaldi, J., Duong, K., Losay, P., Sivakumar, A., Khare, V., et al. (2025) · Cell Transplantation · doi:10.1177/09636897251323966 · Cited by 2
“Indeed, macrophage/microglial activation and neuroinflammation have been shown to contribute to neurodegeneration 55–57 and have been reported to present MPS IIIA 58 , IIIB 58–60 , and IIIC 4,53,61 .”
Ameliorative potential of metformin in LPS and glutamate-induced neurotoxicity in N2a cell-line
Deepshikha, Shekhar, N., Tyagi, S., & Thakur, A. K. (2025) · Cytotechnology · doi:10.1007/s10616-025-00777-9 · Cited by 2
“Exposure of lipopolysaccharides (LPS) as a sturdy stimulator of the microglial cells (Lull and Block 2010) responsible for the initiation of neuronal inflammation, which finally leads to neuronal degeneration (Zheng et al. 2021; Hsiao et al. 2013).”
Health-Promoting Properties of Bioactive Compounds in Edible Mushrooms
Izah, S. C., Jacob, D. E., Ogwu, M. C., & Chime, A. O. (2025) · Reference series in phytochemistry · doi:10.1007/978-3-031-80050-4_2 · Cited by 2
Immunity in Parkinson's disease – The role of innate responses
Iyengar, A. S., Dunkley, P. R., & Dickson, P. W. (2025) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2025.578716 · Cited by 4
Neuroinflammation as a preventive and therapeutic target for postoperative neurocognitive disorders
Kawano, T. (2017) · Journal of the Japanese Society of Intensive Care Medicine · doi:10.3918/jsicm.25_12 · Cited by 2
Ziegenfuss, J. S. (2012) · The Journal of the American Medical Association (JAMA) Network (American Medical Association) · doi:10.13028/7wx4-q868 · Cited by 2
“…is thought to be a feature of diseases ranging from autoimmunity and atherosclerosis to neurological disorders like multiple sclerosis, Alzheimer’s, and Parkinson’s disease (Block et al., 2004; Block et al., 2007; Elliott and Ravichandran, 2010; Linnartz et al., 2010; Lull and Block, 2010).”
BackgroundInfluentialSkaper, S. D. (2017) · Springer eBooks · doi:10.1007/978-3-319-57371-7_12 · Cited by 2
Elgendy, D. I., Othman, A. A., Saied, E. M., & Zoghroban, H. S. (2020) · Journal of the Egyptian Society of Parasitology · doi:10.21608/jesp.2020.130833 · Cited by 2
Chataigner, M., Dinel, A., Pallet, V., Layé, S., & Joffre, C. (2018) · Journal of Alzheimer’s Disease & Parkinsonism · doi:10.4172/2161-0460.1000438 · Cited by 2
“Microglia activation toward the M1 phenotype has been reported to contribute to the neurodegenerative processes and cognition alterations due to the release of proinflammatory mediators and cytokines [228].”
Pathogenesis of Neurodegeneration and Associated Neurological Disorders
Mallhi, T. H., Saifullah, A., Khan, Y. H., Khan, A., Alotaibi, N. H., & Alzarea, A. I. (2021) · Emerging contaminants and associated treatment technologies · doi:10.1007/978-3-030-66376-6_1 · Cited by 1
Mairuae, N., Buranrat, B., Cheepsunth, P., & Yannasithi, S. (2022) · International Journal of Pharmacology · doi:10.3923/ijp.2022.1493.1499 · Cited by 1
Ashwyn, J., Leong, Y. Q., Brianna, B., Ng, K. Y., Chye, S. M., Ling, A. P. K., Voon, K., Ooi, Y. Y., Tiong, Y. L., & Koh, R. Y. (2023) · Pharmaceutical Sciences Asia · doi:10.29090/psa.2023.03.22.333 · Cited by 1
Imam, A. L., Ayodeji, O. A., Sulamon, A. A., Aminu, I., Ibiyeye, R. Y., Adana, M. Y., Omoola, O. O., & Ajao, M. S. (2024) · üha · doi:10.32739/uha.jnbs.11.1539105 · Cited by 1
Impact of sexuality on degenerative diseases
Oyeniran, D. A., Olajide, T. S., Ajagbe͓, A. O., & Mobolaji, A. A. (2025) · Progress in brain research · doi:10.1016/bs.pbr.2025.02.007 · Cited by 1
Chan, P.-M., Tan, Y. S., Chua, K. H., Sabaratnam, V., & Kuppusamy, U. R. (2025) · International journal of medicinal mushrooms · doi:10.1615/intjmedmushrooms.2025058986 · Cited by 1
Health-Promoting Properties of Bioactive Compounds in Edible Mushrooms
Izah, S. C., Jacob, D. E., Ogwu, M. C., & Chime, A. O. (2025) · Reference series in phytochemistry · doi:10.1007/978-3-031-52642-8_2-1 · Cited by 1
Joseph, J. H. M., Irakkam, M. P. B. D., & Kandasamy, M. (2025) · Brain Sciences · doi:10.3390/brainsci15090916 · Cited by 1
“Post-mortem investigations of PD brains have confirmed widespread microglial overactivation, particularly in the SN [43].”
Behera, P., Rangappa, N., Chandrashekar, M., Mishra, A., Chinnathambi, S., & Mishra, M. (2025) · Advances in protein chemistry and structural biology · doi:10.1016/bs.apcsb.2025.08.003 · Cited by 2
Wu, D., Li, X., Xing, Y., Li, Y., Li, Y., Li, C., Wang, Y., Li, H., Liu, J., & Zhang, W. (2025) · Brain Injury · doi:10.1080/02699052.2025.2560587 · Cited by 1
“However, some studies have suggested that astrocytic activation in the amygdala after trauma can induce the overexpression of inflammation-related cytokines associated with pyroptosis, leading to anxiety (12,13).”
Microglia Immunophenotyping in Paraffin Sections of the Brain
Razenkova, V. A., Kirik, O. V., & Korzhevsky, D. E. (2025) · Cell and Tissue Biology · doi:10.1134/s1990519x25600541 · Cited by 1
Annexin A7 enhances TIA1 axonal trafficking to counteract pathological aggregation in neurons
Feng, Y., Luan, T., Zhang, Z., Wang, W., Chu, Y., Wan, S., Pan, X., Li, J., Liu, Y., Xu, Y., et al. (2025) · The EMBO Journal · doi:10.1038/s44318-025-00609-8 · Cited by 2
Protective Effects of Arecoline on LPS-Induced Neuroinflammation in BV2 Microglial Cells
Zhang, X., Cui, J., Sun, J., Fan, B., Wang, F., & Lu, C. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262412097 · Cited by 1
“Over-Int production of NO promotes oxidative stress [37], mitochondrial impairment [38], and neuronal injury [39], and is therefore considered a hallmark of pathological microglial activation [34].”
Liu, Z., Zhang, H., Wan, B., Yin, S., & Yue, R. (2026) · Drug Design Development and Therapy · doi:10.2147/dddt.s580330 · Cited by 2
“158,159 CHR By arresting microglia toward a pro-inflammatory phenotype and downregulating pro-inflammatory cytokine expression, CHR demonstrated neuroprotection and improved the brain plasticity milieu of stroke rats in the chronic phase.”
Kim, C., Nam, M.-K., Yeo, J., Lee, S. H., Jeong, G. H., Lee, J. E., Jung, A., Gweon, B., Yang, S. H., Lim, S. W., et al. (2026) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2026.119755 · Cited by 1
Saiyed, N., Pandya, V. K., Pan, X., Čuperlović‐Culf, M., Ashrafi, N., Kant, S., Migaud, M. E., Dhuguru, J., Zetterberg, H., McGuinness, B., et al. (2026) · npj Aging · doi:10.1038/s41514-025-00324-y · Cited by 1
“These in fl ammatory pro-cessesarefurtherampli fi edbytheactivationofNF-κ Bandthegenerationof peroxynitrite through nitric oxide synthase (iNOS) activity, perpetuating a cycle of neuroin fl ammation and cellular damage 55 – 58 .”
The Arp2/3 complex controls the development of homeostatic microglia
Safaiyan, S., Frosch, M., Bickel, T., Monaco, G., Dvir, R., Madry, C., Bosch, L. F. P., Kierdorf, K., Innocenti, M., Priller, J., et al. (2026) · EMBO Reports · doi:10.1038/s44319-026-00721-8 · Cited by 2
“…lack of morphological transition in Arpc4 - de fi cient microglia coincides with the downregulation of resting and homeostatic genes, which are normally expressed when microglia transform toward the rami fi ed state (Dermitzakis et al, 2023; Lull and Block, 2010; Prinz et al, 2019; Wurm et al, 2021).”
Tau and amyloid-β imaging with proteomics and genomics
Chinnathambi, S., Baisya, U., & Ananthanarayana, V. (2026) · Advances in protein chemistry and structural biology · doi:10.1016/bs.apcsb.2026.02.009 · Cited by 1
Gundapaneni, N., Hill, I., Cheung, L. W. T., Koushki, K., Fausnaught, A. B., Quan, P., Vasan, A. B., Biswal, P., Tripathi, A., Pillai, A., et al. (2026) · Biomedical Microdevices · doi:10.1007/s10544-026-00818-w · Cited by 1
“Persistently activated microglia produce inflam - matory cytokines, which perpetuate inflammation and sup - press neurogenesis, particularly within the hippocampus (Leskinen et al. 2025 ; Lull & Block 2010 ; Makale et al. 2017 ; Monje et al. 2002).”
m6A in RNA: a key regulator of brain development, function and disease
Sivasudhan, E., & Meyer, K. D. (2026) · Nature reviews. Neuroscience · doi:10.1038/s41583-026-01056-y · Cited by 3
“However, prolonged activation leads to the release of pro-inflammatory factors, which can promote neurotoxicity 186,187 .”
Yang, H., Su, B.-W., Bao, Y.-N., Wang, W.-H., Lao, J.-Y., Ji, H.-Y., Han, S., Cui, X.-H., Ren, H.-W., & Luan, Z.-L. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1880374 · Cited by 1
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“While they are essential for synaptic plasticity and debris clearance [32], chronic microglial activation contributes to sustained neuroinflammation, releasing cytokines and reactive oxygen species (ROS) that exacerbate neuronal vulnerability [67].”
Microglia, Calcification and Neurodegenerative Diseases
Jose, M., Mahy, N., & Manuel, J. (2011) · InTech eBooks · doi:10.5772/28464 · Cited by 1
“In contrast, once microglia become overactivated they can produce detrimental effects through excessive production of a large array of cytotoxic factors, such as NO, TNF-α, reactive oxygen species, and pro-inflammatory cytokines (Lull & Block, 2010, Milligan & Watkins, 2009).”
Background(2014) · Inflammation and Cell Signaling · doi:10.14800/ics.226 · Cited by 1
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Metadata
- Authors
- Lull, M. E., & Block, M. L.
- Affiliations
- Virginia Commonwealth University (US)
- Corresponding author
- Block, Michelle L.
- Venue
- Neurotherapeutics
- Publisher
- Elsevier BV
- Published
- 2010-10
- Volume
- 7
- Issue
- 4
- Pages
- 354-365
- ISSN
- 1878-7479 (ISSN-L)
- PMC
- PMC2951017
- OpenAlex
- W2050320551
- Cited by
- 1,047
- References
- 182
- Citations by year
- 2026: 50 · 2025: 112 · 2024: 94 · 2023: 60 · 2022: 84 · 2021: 95 · 2020: 84 · 2019: 78 · 2018: 83 · 2017: 76 · 2016: 73 · 2015: 43 · 2014: 38 · 2013: 28 · 2012: 30
- FWCI
- 14.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neurotherapeutics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Fisher Digital Publications (St. John Fisher College) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Environmental Health Sciences (R01ES016951, R00ES01549)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- microglial activation, neurodegeneration, reactive microgliosis, reactive oxygen species, neuroinflammation, neurotoxicity, Parkinson's disease, neuronal cell death, lipopolysaccharide, TNF-α, nitric oxide, IL-1β
- MeSH terms
- Animals, Chronic Disease, Dopamine, Humans, Models, Biological, Neurons, Oxidation-Reduction, Signal Transduction, Reactive Oxygen Species, Microglia, NADPH Oxidases, Neurodegenerative Diseases
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