Toll-Like Receptor 4 Promotes α-Synuclein Clearance and Survival of Nigral Dopaminergic Neurons
Open accessAbstract
Toll-like receptors (TLRs) mediate innate immunity, and their dysregulation may play a role in α-synucleinopathies, such as Parkinson's disease or multiple system atrophy (MSA). The aim of this study was to define the role of TLR4 in α-synuclein-linked neurodegeneration. Ablation of TLR4 in a transgenic mouse model of MSA with oligodendroglial α-synuclein overexpression augmented motor disability and enhanced loss of nigrostriatal dopaminergic neurons. These changes were associated with increased brain levels of α-synuclein linked to disturbed TLR4-mediated microglial phagocytosis of α-synuclein. Furthermore, tumor necrosis factor-α levels were increased in the midbrain and associated with a proinflammatory astroglial response. Our data suggest that TLR4 ablation impairs the phagocytic response of microglia to α-synuclein and enhances neurodegeneration in a transgenic MSA mouse model. The study supports TLR4 signaling as innate neuroprotective mechanism acting through clearance of α-synuclein.
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TLR4 is required for increased inflammation in response to various forms of α-synuclein.
“TLR4 was required for NF-κB activation, and increased inflammation and phagocytic activity in response to various forms of α-synuclein40,41,56.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [56]
The Results section reports the opposite for an inflammatory measure: α-synuclein-overexpressing mice lacking TLR4 had increased midbrain TNF-α and a proinflammatory astroglial response. The Discussion supports a role for TLR4 in α-synuclein phagocytosis, but not the attributed requirement for increased inflammation. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredTLR4 is required for increased phagocytic activity in response to various forms of α-synuclein.
“TLR4 was required for NF-κB activation, and increased inflammation and phagocytic activity in response to various forms of α-synuclein40,41,56.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [56]
TLR4 is required for NF-κB activation in response to various forms of α-synuclein.
“TLR4 was required for NF-κB activation, and increased inflammation and phagocytic activity in response to various forms of α-synuclein40,41,56.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [56]
The Discussion reports that TLR4 mediates microglial phagocytosis of α-synuclein, but it does not address the cited claim about NF-κB activation. Searches for NF-κB, NF-kappaB, and responses to different α-synuclein forms found no passage establishing that TLR4 is required for that activation. (LLM, conf=0.72)
Experimental — accuracy not yet measuredTLR4 gene ablation in a transgenic mouse model of MSA with oligodendroglial α-syn overexpression impaired microglial phagocytic ability for α-syn, leading to enhanced motor impairment and augmented loss of nigrostriatal dopaminergic neurons.
“TLR4 gene ablation in a transgenic mouse model of MSA with oligodendroglial α-syn overexpression impaired the phagocytic ability of microglia to α-syn, leading to enhanced motor impairment and augmented loss of nigrostriatal dopaminergic neurons.295”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [295]
In MSA brains, increased brain levels of α-syn were linked to disturbed TLR4-mediated microglial phagocytosis of α-syn.
“In MSA brains, increased brain levels of α-syn were linked to disturbed TLR4-mediated microglial phagocytosis of α-syn.295”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [295]
A mouse model with lentiviral-mediated selective α-syn accumulation in microglial cells in the substantia nigra developed progressive degeneration of dopaminergic neurons.
“A study generated a mouse model by lentiviral-mediated selective α-syn accumulation in microglial cells in substantia nigra and found that these mice developed progressive degeneration of dopaminergic neurons.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [295]
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- Authors
- Stefanova, N., Fellner, L., Reindl, M., Masliah, E., Poewe, W., & Wenning, G. K.
- Affiliations
- Innsbruck Medical University (AT)
- University of California San Diego (US)
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2011-08
- Volume
- 179
- Issue
- 2
- Pages
- 954-963
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC3157205
- OpenAlex
- W2078504890
- Cited by
- 272
- References
- 65
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 18 · 2023: 17 · 2022: 24 · 2021: 29 · 2020: 29 · 2019: 20 · 2018: 25 · 2017: 22 · 2016: 14 · 2015: 10 · 2014: 13 · 2013: 15 · 2012: 13
- FWCI
- 8.52
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AG022074, AG18440, AG5131, NS057096, NS044233)
- Austrian Science Fund (P19989-B05, SFB F44-B19)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- TLR4, alpha-synuclein, multiple system atrophy, Parkinson's disease, nigrostriatal dopaminergic neurons, microglial phagocytosis, neurodegeneration, TNF-α, astroglial response, innate immunity, neuroprotection
- MeSH terms
- Animals, Behavior, Animal, Enzyme-Linked Immunosorbent Assay, Inflammation, Mice, Inbred C57BL, Mice, Transgenic, Models, Biological, Phenotype, Substantia Nigra, DNA Primers, Microscopy, Confocal, Neurodegenerative Diseases, Cell Line, Tumor, Toll-Like Receptor 4, Mice, alpha-Synuclein, Dopaminergic Neurons
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