ArticleTranslational neurodegeneration2024
Increased cysteinyl-tRNA synthetase drives neuroinflammation in Alzheimer's disease.
Article in Translational neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Mitochondrial enzyme dysfunction in Alzheimer's disease: a systematic review of human metabolic evidence.Metabolic brain disease · 2026Pooled it
- 10,11-Dehydrocurvularin attenuates LPS-induced neuroinflammation in BV2 cells by inhibiting the TLR2/MyD88/NLRP3 signaling pathway.Biochemistry and biophysics reports · 2026Article
- Human aminoacyl-tRNA synthetases as integrators of translation and cell signalling networks.Nature reviews. Molecular cell biology · 2026Review
- Identification and validation of CARS1 p.E712V and NF1 p.Q2002X in sporadic Moyamoya disease across 30 trio pedigrees.NPJ genomic medicine · 2026Article
- Lupeol restores dopaminergic function by suppressing glial activation in a Parkinson's disease mouse model.Frontiers in immunology · 2026Article
- Shannon Entropy of Gray Matter Eigenmodes: A Novel Biomarker for Alzheimer's Disease and Heterogeneous MCI Trajectories.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microglia-Neuron Interactions in Alzheimer's Disease.Current neuropharmacology · 2026Review
- Secreted mitochondrial aspartyl-tRNA synthetase (DARS2) regulates TNFα signaling.Physiological reports · 2025Article
- Anatomical mapping of GFAP-immunoreactive astrocytes in the tree shrew brain.Zoological research · 2025Article
- Serine mistranslation induces the integrated stress response through the P stalk.The Journal of biological chemistry · 2025Article
- Decoding tRNA dynamics in neuroimmune disorders: mechanistic insights, diagnostic innovations, and therapeutic opportunities.Frontiers in immunology · 2025Review
- The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- Investigating the Neuroprotective and Cognitive-Enhancing Effects ofAntioxidants (Basel, Switzerland) · 2024Review
- Epigenetic modifications of DNA and RNA in Alzheimer's disease.Frontiers in molecular neuroscience · 2024Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundMicroglia-mediated neuroinflammation in Alzheimer's disease (AD) is not only a response to pathophysiological events, but also plays a causative role in neurodegeneration. Cytoplasmic cysteinyl-tRNA synthetase (CARS) is considered to be a stimulant for immune responses to diseases; however, it remains unknown whether CARS is involved in the pathogenesis of AD.
methodsPostmortem human temporal cortical tissues at different Braak stages and AD patient-derived serum samples were used to investigate the changes of CARS levels in AD by immunocytochemical staining, real-time PCR, western blotting and ELISA. After that, C57BL/6J and APP/PS1 transgenic mice and BV-2 cell line were used to explore the role of CARS protein in memory and neuroinflammation, as well as the underlying mechanisms. Finally, the associations of morphological features among CARS protein, microglia and dense-core plaques were examined by immunocytochemical staining.
resultsA positive correlation was found between aging and the intensity of CARS immunoreactivity in the temporal cortex. Both protein and mRNA levels of CARS were increased in the temporal cortex of AD patients. Immunocytochemical staining revealed increased CARS immunoreactivity in neurons of the temporal cortex in AD patients. Moreover, overexpression of CARS in hippocampal neurons induced and aggravated cognitive dysfunction in C57BL/6J and APP/PS1 mice, respectively, accompanied by activation of microglia and the TLR2/MyD88 signaling pathway as well as upregulation of proinflammatory cytokines. In vitro experiments showed that CARS treatment facilitated the production of proinflammatory cytokines and the activation of the TLR2/MyD88 signaling pathway of BV-2 cells. The accumulation of CARS protein occurred within dense-core Aβ plaques accompanied by recruitment of ameboid microglia. Significant upregulation of TLR2/MyD88 proteins was also observed in the temporal cortex of AD.
conclusionsThe findings suggest that the neuronal CARS drives neuroinflammation and induces memory deficits, which might be involved in the pathogenesis of AD.
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Registered trials
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