Blockade of STING activation alleviates microglial dysfunction and a broad spectrum of Alzheimer’s disease pathologies

Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia a...

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Published inExperimental & molecular medicine Vol. 56; no. 9; pp. 1936 - 1951
Main Authors Chung, Sunwoo, Jeong, June-Hyun, Park, Jong-Chan, Han, Jong Won, Lee, Yeajina, Kim, Jong-Il, Mook-Jung, Inhee
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.09.2024
Springer Nature B.V
Nature Publishing Group
생화학분자생물학회
Subjects
13/100
14/19
45/91
631/378/1689/1283
631/378/371
64/110
82/51
82/80
Alzheimer Disease - etiology
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Animals
Apolipoprotein E
Artificial intelligence
Biomedical and Life Sciences
Biomedicine
Brain
Brain injury
Cytoplasm
Dementia disorders
Disease Models, Animal
Gliosis
Humans
Immune response
Immunological memory
Inflammation
Medical Biochemistry
Membrane Proteins - genetics
Membrane Proteins - metabolism
Memory
Mice
Mice, Transgenic
Microglia
Microglia - metabolism
Microglia - pathology
Mitochondrial DNA
Molecular Medicine
Neurodegeneration
Neurodegenerative diseases
Neuronal-glial interactions
Nucleotidyltransferases - genetics
Nucleotidyltransferases - metabolism
Phosphorylation
Proteins
Risk factors
Signal Transduction
Stem Cells
Synapses
Tau protein
Therapeutic targets
Transcriptomes
β-Amyloid
생화학
Online AccessGet full text
ISSN2092-6413
1226-3613
2092-6413
DOI10.1038/s12276-024-01295-y

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Abstract Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in App NL-G-F /hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD. STING inhibition mitigates neurodegeneration in Alzheimer’s disease In illnesses like Alzheimer’s that cause brain deterioration, the brain’s defense cells, known as microglia, overreact due to harmful proteins, causing brain damage and memory loss. This research aimed to understand how microglia change in Alzheimer’s and find ways to stop their damaging effects. Using mice with Alzheimer’s, they checked if blocking specific immune pathway could fix microglia dysfunction and Alzheimer’s disease pathologies. They discovered that blocking STING, a crucial part of this pathway, reduced microglia dysfunction brain inflammation, decreased the buildup of Alzheimer’s-related proteins, and improved memory in mice. By blocking the STING activation, the study showed a decrease in damaging brain inflammation and improvements in memory function, suggesting a promising strategy for treating Alzheimer’s. Researchers conclude that targeting the STING could offer a new way to fight Alzheimer’s by reducing inflammation and protecting brain health. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
AbstractList Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in App NL-G-F /hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD. STING inhibition mitigates neurodegeneration in Alzheimer’s disease In illnesses like Alzheimer’s that cause brain deterioration, the brain’s defense cells, known as microglia, overreact due to harmful proteins, causing brain damage and memory loss. This research aimed to understand how microglia change in Alzheimer’s and find ways to stop their damaging effects. Using mice with Alzheimer’s, they checked if blocking specific immune pathway could fix microglia dysfunction and Alzheimer’s disease pathologies. They discovered that blocking STING, a crucial part of this pathway, reduced microglia dysfunction brain inflammation, decreased the buildup of Alzheimer’s-related proteins, and improved memory in mice. By blocking the STING activation, the study showed a decrease in damaging brain inflammation and improvements in memory function, suggesting a promising strategy for treating Alzheimer’s. Researchers conclude that targeting the STING could offer a new way to fight Alzheimer’s by reducing inflammation and protecting brain health. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
Abstract Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in AppNL-G-F/hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD.
Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in AppNL-G-F/hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD. KCI Citation Count: 15
Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in AppNL-G-F/hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD.STING inhibition mitigates neurodegeneration in Alzheimer’s diseaseIn illnesses like Alzheimer’s that cause brain deterioration, the brain’s defense cells, known as microglia, overreact due to harmful proteins, causing brain damage and memory loss. This research aimed to understand how microglia change in Alzheimer’s and find ways to stop their damaging effects. Using mice with Alzheimer’s, they checked if blocking specific immune pathway could fix microglia dysfunction and Alzheimer’s disease pathologies. They discovered that blocking STING, a crucial part of this pathway, reduced microglia dysfunction brain inflammation, decreased the buildup of Alzheimer’s-related proteins, and improved memory in mice. By blocking the STING activation, the study showed a decrease in damaging brain inflammation and improvements in memory function, suggesting a promising strategy for treating Alzheimer’s. Researchers conclude that targeting the STING could offer a new way to fight Alzheimer’s by reducing inflammation and protecting brain health.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in AppNL-G-F/hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD. In illnesses like Alzheimer’s that cause brain deterioration, the brain’s defense cells, known as microglia, overreact due to harmful proteins, causing brain damage and memory loss. This research aimed to understand how microglia change in Alzheimer’s and find ways to stop their damaging effects. Using mice with Alzheimer’s, they checked if blocking specific immune pathway could fix microglia dysfunction and Alzheimer’s disease pathologies. They discovered that blocking STING, a crucial part of this pathway, reduced microglia dysfunction brain inflammation, decreased the buildup of Alzheimer’s-related proteins, and improved memory in mice. By blocking the STING activation, the study showed a decrease in damaging brain inflammation and improvements in memory function, suggesting a promising strategy for treating Alzheimer’s. Researchers conclude that targeting the STING could offer a new way to fight Alzheimer’s by reducing inflammation and protecting brain health. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
Abnormal glial activation promotes neurodegeneration in Alzheimer's disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in AppNL-G-F/hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD.Abnormal glial activation promotes neurodegeneration in Alzheimer's disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in AppNL-G-F/hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD.
Abnormal glial activation promotes neurodegeneration in Alzheimer's disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in App /hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD.
Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD. We showed that inhibiting STING activation can control microglia and ameliorate a wide spectrum of AD symptoms. The cGAS-STING pathway is required for the detection of ectopic DNA and the subsequent immune response. Amyloid-β (Aβ) and tau induce mitochondrial stress, which causes DNA to be released into the cytoplasm of microglia. cGAS and STING are highly expressed in Aβ plaque-associated microglia, and neuronal STING is upregulated in the brains of AD model animals. The presence of the APOE ε4 allele, an AD risk factor, also upregulated both proteins. STING activation was necessary for microglial NLRP3 activation, proinflammatory responses, and type-I-interferon responses. Pharmacological STING inhibition reduced a wide range of AD pathogenic features in App NL-G-F /hTau double-knock-in mice. An unanticipated transcriptome shift in microglia reduced gliosis and cerebral inflammation. Significant reductions in the Aβ load, tau phosphorylation, and microglial synapse engulfment prevented memory loss. To summarize, our study describes the pathogenic mechanism of STING activation as well as its potential as a therapeutic target in AD.
Author Lee, Yeajina
Mook-Jung, Inhee
Kim, Jong-Il
Park, Jong-Chan
Jeong, June-Hyun
Han, Jong Won
Chung, Sunwoo
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Snippet Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway...
Abnormal glial activation promotes neurodegeneration in Alzheimer's disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING pathway...
Abstract Abnormal glial activation promotes neurodegeneration in Alzheimer’s disease (AD), the most common cause of dementia. Stimulation of the cGAS-STING...
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SubjectTerms 13/100
14/19
45/91
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64/110
82/51
82/80
Alzheimer Disease - etiology
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Animals
Apolipoprotein E
Artificial intelligence
Biomedical and Life Sciences
Biomedicine
Brain
Brain injury
Cytoplasm
Dementia disorders
Disease Models, Animal
Gliosis
Humans
Immune response
Immunological memory
Inflammation
Medical Biochemistry
Membrane Proteins - genetics
Membrane Proteins - metabolism
Memory
Mice
Mice, Transgenic
Microglia
Microglia - metabolism
Microglia - pathology
Mitochondrial DNA
Molecular Medicine
Neurodegeneration
Neurodegenerative diseases
Neuronal-glial interactions
Nucleotidyltransferases - genetics
Nucleotidyltransferases - metabolism
Phosphorylation
Proteins
Risk factors
Signal Transduction
Stem Cells
Synapses
Tau protein
Therapeutic targets
Transcriptomes
β-Amyloid
생화학
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Title Blockade of STING activation alleviates microglial dysfunction and a broad spectrum of Alzheimer’s disease pathologies
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