The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Microglia centered pathogenesis in ALS: insights in cell interconnectivity
Open accessAbstract
Amyotrophic lateral sclerosis (ALS) is the most common and most aggressive form of adult motor neuron (MN) degeneration. The cause of the disease is still unknown, but some protein mutations have been linked to the pathological process. Loss of upper and lower MNs results in progressive muscle paralysis and ultimately death due to respiratory failure. Although initially thought to derive from the selective loss of MNs, the pathogenic concept of non-cell-autonomous disease has come to the forefront for the contribution of glial cells in ALS, in particular microglia. Recent studies suggest that microglia may have a protective effect on MN in an early stage. Conversely, activated microglia contribute and enhance MN death by secreting neurotoxic factors, and impaired microglial function at the end-stage may instead accelerate disease progression. However, the nature of microglial-neuronal interactions that lead to MN degeneration remains elusive. We review the contribution of the neurodegenerative network in ALS pathology, with a special focus on each glial cell type from data obtained in the transgenic SOD1G93A rodents, the most widely used model. We further discuss the diverse roles of neuroinflammation and microglia phenotypes in the modulation of ALS pathology. We provide information on the processes associated with dysfunctional cell-cell communication and summarize findings on pathological cross-talk between neurons and astroglia, and neurons and microglia, as well as on the spread of pathogenic factors. We also highlight the relevance of neurovascular disruption and exosome trafficking to ALS pathology. The harmful and beneficial influences of NG2 cells, oligodendrocytes and Schwann cells will be discussed as well. Insights into the complex intercellular perturbations underlying ALS, including target identification, will enhance our efforts to develop effective therapeutic approaches for preventing or reversing symptomatic progression of this devastating disease.
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BackgroundA Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD
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BackgroundA new class of membrane-bound chemokine with a CX3C motif
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Cited by
Microglia in physiology and disease
Wolf, S. A., Boddeke, H. W. G. M., & Kettenmann, H. (2017) · Annual Review of Physiology · doi:10.1146/annurev-physiol-022516-034406 · Cited by 1,426
Brites, D., & Fernandes, A. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00476 · Cited by 599
“, 2015); and (iii) M2c associated with phagocytosis and suppression of the innate immune system (Brites and Vaz, 2014).”
BackgroundInfluentialSelf-citationThe Impact of the CX3CL1/CX3CR1 Axis in Neurological Disorders
Pawelec, P., Ziemka-Nalecz, M., Sypecka, J., & Zalewska, T. (2020) · Cells · doi:10.3390/cells9102277 · Cited by 269
The microglial NLRP3 inflammasome is activated by amyotrophic lateral sclerosis proteins
Deora, V., Lee, J. D., Albornoz, E. A., McAlary, L., Jagaraj, C. J., Robertson, A. A. B., Atkin, J. D., Cooper, M. A., Schroder, K., Yerbury, J. J., et al. (2020) · Glia · doi:10.1002/glia.23728 · Cited by 245
Exploring New Inflammatory Biomarkers and Pathways during LPS-Induced M1 Polarization
Cunha, C., Gomes, C., Vaz, A. R., & Brites, D. (2016) · Mediators of Inflammation · doi:10.1155/2016/6986175 · Cited by 153
Self-citation
Metadata
- Authors
- Brites, D., & Vaz, A. R.
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2014-05-22
- Volume
- 8
- Pages
- 117-117
- ISSN
- 1662-5102 (ISSN-L)
- OpenAlex
- W2065894198
- Cited by
- 203
- References
- 41
- FWCI
- 13.19
- Type
- journal article
- Language
- en
- Open access
- gold
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
