ArticleScientific reports2015
Neuroinflammation and Aβ accumulation linked to systemic inflammation are decreased by genetic PKR down-regulation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 91 citations in OpenAlex.
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- Increased neurotoxic gliosis and blood-brain barrier dysregulation in canine cognitive dysfunction syndrome (CCD).Frontiers in aging · 2026Article
- A neurodegenerative cellular stress response linked to dark microglia and toxic lipid secretion.Neuron · 2025Article
- PKR Inhibition Prevents Neuroinflammation and Rescues Depressive-Like Behaviors via BDNF/TrkB Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Article
- PKR modulates sterile systemic inflammation-triggered neuroinflammation and brain glucose metabolism disturbances.Frontiers in immunology · 2025Article
- Investigation of Novel Aronia Bioactive Fraction-Alginic Acid Nanocomplex on the Enhanced Modulation of Neuroinflammation and Inhibition of Aβ Aggregation.Pharmaceutics · 2024Article
- Another Use for a Proven Drug: Experimental Evidence for the Potential of Artemisinin and Its Derivatives to Treat Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Novel targets and therapies of metformin in dementia: old drug, new insights.Frontiers in pharmacology · 2024Review
- Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review).International journal of molecular medicine · 2023Review
- Sex-specific relationship between non-alcoholic fatty liver disease and amyloid-β in cognitively unimpaired individuals.Frontiers in aging neuroscience · 2023Article
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- APOE4 confers transcriptomic and functional alterations to primary mouse microglia.Neurobiology of disease · 2022Article
- Protein kinase R is an innate immune sensor of proteotoxic stress via accumulation of cytoplasmic IL-24.Science immunology · 2022Article
- Immunoproteasomes control activation of innate immune signaling and microglial function.Frontiers in immunology · 2022Article
- Neuroinflammation in neurodegenerationFrontiers in immunology · 2022Review
- Supplementation of Carvacrol Attenuates Hippocampal Tumor Necrosis Factor-Alpha Level, Oxidative Stress, and Learning and Memory Dysfunction in Lipopolysaccharide-Exposed Rats.Advanced biomedical research · 2022Article
- A Diagnostic Model for Alzheimer's Disease Based on Blood Levels of Autophagy-Related Genes.Frontiers in aging neuroscience · 2022Article
- Non-Alcoholic Fatty Liver Disease, Liver Fibrosis, and Regional Amyloid-β and Tau Pathology in Middle-Aged Adults: The Framingham Study.Journal of Alzheimer's disease : JAD · 2022Article
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder, marked by senile plaques composed of amyloid-β (Aβ) peptide, neurofibrillary tangles, neuronal loss and neuroinflammation. Previous works have suggested that systemic inflammation could contribute to neuroinflammation and enhanced Aβ cerebral concentrations. The molecular pathways leading to these events are not fully understood. PKR is a pro-apoptotic kinase that can trigger inflammation and accumulates in the brain and cerebrospinal fluid of AD patients. The goal of the present study was to assess if LPS-induced neuroinflammation and Aβ production could be altered by genetic PKR down regulation. The results show that, in the hippocampus of LPS-injected wild type mice, neuroinflammation, cytokine release and Aβ production are significantly increased and not in LPS-treated PKR knock-out mice. In addition BACE1 and activated STAT3 levels, a putative transcriptional regulator of BACE1, were not found increased in the brain of PKR knock-out mice as observed in wild type mice. Using PET imaging, the decrease of hippocampal metabolism induced by systemic LPS was not observed in LPS-treated PKR knock-out mice. Altogether, these findings demonstrate that PKR plays a major role in brain changes induced by LPS and could be a valid target to modulate neuroinflammation and Aβ production.
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