Neurodegeneration and NLRP3 inflammasome expression in the anterior thalamus of SOD1(G93A) ALS mice
Open accessAbstract
Nowadays, amyotrophic lateral sclerosis (ALS) is considered as a multisystem disorder, characterized by a primary degeneration of motor neurons as well as neuropathological changes in non-motor regions. Neurodegeneration in subcortical areas, such as the thalamus, are believed to contribute to cognitive and behavioral abnormalities in ALS patients. In the present study, we investigated neurodegenerative changes including neuronal loss and glia pathology in the anterodorsal thalamic nucleus (AD) of SOD1(G93A) mice, a widely used animal model for ALS. We detected massive dendrite swelling and neuronal loss in SOD1(G93A) animals, which was accompanied by a mild gliosis. Furthermore, misfolded SOD1 protein and autophagy markers were accumulating in the AD. Since innate immunity and activation inflammasomes seem to play a crucial role in ALS, we examined protein expression of Nod-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase-1 recruitment domain (ASC) and the cytokine interleukin 1 beta (IL1β) in AD glial cells and neurons. NLRP3 and ASC were significantly up-regulated in the AD of SOD1(G93A) mice. Finally, co-localization studies revealed expression of NLRP3, ASC and IL1β in neurons. Our study yielded two main findings: (i) neurodegenerative changes already occur at an early symptomatic stage in the AD and (ii) increased inflammasome expression may contribute to neuronal cell death. In conclusion, neurodegeneration in the anterior thalamus may critically account for cognitive changes in ALS pathology.
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Expression of NLRP3 and ASC was greatly increased in the anterodorsal thalamic nucleus of an ALS mouse model.
“Moreover, the expression of NLRP3 and ASC was greatly increased in the anterodorsal thalamic nucleus of ALS mouse model.367”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [367]
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“Moreover, the expression of NLRP3 and ASC was greatly increased in the anterodorsal thalamic nucleus of ALS mouse model.(367) The NLRP3 inflammasome in microglia was also involved in TDP-43-induced toxicity to motor neurons.”
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- Authors
- Debye, B., Schmülling, L., Zhou, L., Rune, G., Beyer, C., & Johann, S.
- Affiliations
- RWTH Aachen University (DE)
- University Medical Center Hamburg-Eppendorf (DE)
- Corresponding author
- Johann, Sonja
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2017-03-22
- Volume
- 28
- Issue
- 1
- Pages
- 14-27
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC8028558
- OpenAlex
- W2551371786
- Cited by
- 81
- References
- 85
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 10 · 2023: 5 · 2022: 16 · 2021: 10 · 2020: 9 · 2019: 5 · 2018: 4 · 2017: 5
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyotrophic lateral sclerosis, NLRP3 inflammasome, anterior thalamic nuclei, anterodorsal thalamic nucleus, SOD1 G93A mice, neurodegeneration, neuronal loss, gliosis, autophagy, ASC, IL-1β, innate immunity, cognitive impairment
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Superoxide Dismutase-1, Amyotrophic Lateral Sclerosis, Animals, Disease Models, Animal, Female, Humans, Male, Mice, Transgenic, Nerve Degeneration, Neuroglia, Neurons, Cell Death, Disease Progression, Anterior Thalamic Nuclei, CARD Signaling Adaptor Proteins, Interleukin-1beta, Inflammasomes
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