ArticleBrain pathology (Zurich, Switzerland)2018
Neurodegeneration and NLRP3 inflammasome expression in the anterior thalamus of SOD1(G93A) ALS mice.
Article in Brain pathology (Zurich, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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49 citing papers in PubMed, 87 citations in OpenAlex.
- Innate immune crosstalk in ALS/FTD pathogenesis.Cell insight · 2026Review
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- 3D Artificial Skin Model As a Novel Strategy for the Detection of Pyroptosis-Cascade Activation in Amyotrophic Lateral Sclerosis.ACS applied materials & interfaces · 2026Article
- A Putative Role for the BCL2 Family of Proteins in the Pathophysiology of ALS.CNS & neurological disorders drug targets · 2026Article
- Effects of exercise on neuroinflammation in age-related neurodegenerative disorders.European journal of medical research · 2025Review
- The Emerging Role of the Brain-Gut Axis in Amyotrophic Lateral Sclerosis: Pathogenesis, Mechanisms, and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- Long-term impact of white matter hyperintensities and amyloid beta on thalamic subregions in cerebral small vessel disease: A prospective cohort study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Circulating miR-223/NLRP3 axis and IL-1β level in functional disease progression of amyotrophic lateral sclerosis.Acta neurologica Belgica · 2025Article
- Targeting inflammasome pathway towards therapeutics of neurodegenerative diseases.Organelle (Tucson, Ariz.) · 2025Article
- Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- VCP Inhibition Augments NLRP3 Inflammasome Activation.Inflammation · 2024Article
- Mitophagy and cGAS-STING crosstalk in neuroinflammation.Acta pharmaceutica Sinica. B · 2024Review
- Elevated NLRP3 Inflammasome Activation Is Associated with Motor Neuron Degeneration in ALS.Cells · 2024Article
- Desloratadine alleviates ALS-like pathology in hSOD1Acta pharmacologica Sinica · 2024Article
- Brain-Gut-Microbiota Axis in Amyotrophic Lateral Sclerosis: A Historical Overview and Future Directions.Aging and disease · 2024Review
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Article
- Targeting NLRP3 inflammasome for neurodegenerative disorders.Molecular psychiatry · 2023Review
- The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death.Biomedicines · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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