The DOI matches its Crossref record; 181 of the 182 references it cites were found in a registry or an index.
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
Experimental — accuracy not yet measuredIn the citing paper
“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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Citations
Cites
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
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Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
Nimmerjahn, A., Kirchhoff, F., & Helmchen, F. (2005) · Science · doi:10.1126/science.1110647 · Cited by 5,827 · cited 1×
“Despite the fact that these ramified microglia are referred to as resting, they are constantly surveying the surrounding environment by extending and retracting their processes.(23,24) In doing this, microglia are able to sample the microenvironment, maintain homeostasis, and identify signals that require a response.”
BackgroundChronic Parkinsonism in Humans Due to a Product of Meperidine-Analog Synthesis
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Microglia: a sensor for pathological events in the CNS
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“When reacting to extracellular signals, such as the presence of pathogens, foreign material, and dead or dying cells, microglia may undergo a morphological change into an ameboid shape with short or nonexistent processes.(25) This morphological change is also accompanied by changes in signaling and gene expression tha…”
BackgroundMicroglia-mediated neurotoxicity: uncovering the molecular mechanisms
Block, M. L., Zecca, L., & Hong, J.-S. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2038 · Cited by 4,110 · cited 2×
“Reactive microgliosis-chronic response to a single stimulus Although microglial activation was initially perceived as a transient event,(31) it is now believed to be chronic and culpable in the propagation of disease.(1,94,157) Reports have shown that microglia can remain chronically activated(140,158,159) in a proces…”
BackgroundSelf-citationATP mediates rapid microglial response to local brain injury in vivo
Davalos, D., Grutzendler, J., Yang, G., Kim, J. V., Zuo, Y., Jung, S., Littman, D. R., Dustin, M. L., & Gan, W.-B. (2005) · Nature Neuroscience · doi:10.1038/nn1472 · Cited by 3,913 · cited 1×
“Despite the fact that these ramified microglia are referred to as resting, they are constantly surveying the surrounding environment by extending and retracting their processes.(23,24) In doing this, microglia are able to sample the microenvironment, maintain homeostasis, and identify signals that require a response.”
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Blood Monocytes Consist of Two Principal Subsets with Distinct Migratory Properties
Geissmann, F., Jung, S., & Littman, D. R. (2003) · Immunity · doi:10.1016/s1074-7613(03)00174-2 · Cited by 3,504
Reactive oxygen species, cellular redox systems, and apoptosis
Circu, M. L., & Aw, T. Y. (2010) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.12.022 · Cited by 3,340
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Research works printed but not linked: 2
- Wu, 2005, The role of microglia in paraquat-induced dopaminergic neurotoxicity, Antioxid Redox Signal, 7, 654, 10.1089/ars.2005.7.654 · DOI
- Niehaus, 2003, Lippopolysaccharides induce inflammation-mediated neurodeheneration in the substantia nigra and the cerebral cortex (A case report), AD/PD 6th International Conference, 1
Cited by
Sorted by citations
Zielonka, J., Joseph, J., Sikora, A., Hardy, M., Ouari, O., Vasquez-Vivar, J., Cheng, G., Lopez, M., & Kalyanaraman, B. (2017) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00042 · Cited by 1,683
Role of neuroinflammation in neurodegenerative diseases (Review)
Chen, W., Zhang, X., & Huang, W. (2016) · Molecular Medicine Reports · doi:10.3892/mmr.2016.4948 · Cited by 961
“However, inflammation in tissue pathology that may result in the production of neurotoxic factors amplifying the disease states, indicates the persistence of inflammatory stimuli or failure in normal resolution mechanisms (16,17).”
Paracrine Mechanisms of Mesenchymal Stem Cell-Based Therapy: Current Status and Perspectives
Liang, X., Ding, Y., Zhang, Y., Tse, H.-F., & Lian, Q. (2014) · Cell Transplantation · doi:10.3727/096368913x667709 · Cited by 909
Neuroinflammation as a common feature of neurodegenerative disorders
Guzman-Martinez, L., Maccioni, R. B., Andrade, V., Navarrete, L. P., Pastor, M. G., & Ramos-Escobar, N. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.01008 · Cited by 702
Jiang, T., Sun, Q., & Chen, S. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.07.005 · Cited by 605
“OS is thought to be the underlying etiology that leads to cellular dysfunction and demise in both idiopathic and genetic cases of PD (Hwang, 2013; Lull and Block, 2010).”
Background
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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