ArticleInternational journal of Alzheimer's disease2013
Alpha 1-Antichymotrypsin, an Inflammatory Protein Overexpressed in the Brains of Patients with Alzheimer's Disease, Induces Tau Hyperphosphorylation through c-Jun N-Terminal Kinase Activation.
Article in International journal of Alzheimer's disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Multi-omic analysis of Huntington's disease reveals a compensatory astrocyte state.Nature communications · 2024Article
- Multi-OMIC analysis of Huntington disease reveals a neuroprotective astrocyte state.bioRxiv : the preprint server for biology · 2023Article
- Hippocampal delivery of neurotrophic factor-α1/carboxypeptidase E gene prevents neurodegeneration, amyloidosis, memory loss in Alzheimer's Disease male mice.Molecular psychiatry · 2023Article
- Traumatic brain injury and the pathways to cerebral tau accumulation.Frontiers in neurology · 2023Review
- Toxicities of amyloid-beta and tau protein are reciprocally enhanced in theNeural regeneration research · 2022Article
- Novel Exosome Biomarker Candidates for Alzheimer's Disease Unravelled Through Mass Spectrometry Analysis.Molecular neurobiology · 2022Article
- Alpha-1-antichymotrypsin as a novel biomarker for diagnosis, prognosis, and therapy prediction in human diseases.Cancer cell international · 2022Review
- Revelation of Pivotal Genes Pertinent to Alzheimer's Pathogenesis: A Methodical Evaluation of 32 GEO Datasets.Journal of molecular neuroscience : MN · 2022Article
- Transcriptome and Translatome Regulation of Pathogenesis in Alzheimer's Disease Model Mice.Journal of Alzheimer's disease : JAD · 2022Article
- Clioquinol Decreases Levels of Phosphorylated, Truncated, and Oligomerized Tau Protein.International journal of molecular sciences · 2021Article
- Serpins in cartilage and osteoarthritis: what do we know?Biochemical Society transactions · 2021Review
- Exosomal Aβ-Binding Proteins Identified by "In Silico" Analysis Represent Putative Blood-Derived Biomarker Candidates for Alzheimer´s Disease.International journal of molecular sciences · 2021Article
- Alpha 1-antichymotrypsin may be a biomarker for the progression of amnestic mild cognitive impairment.Acta neurologica Belgica · 2021Article
- Prediction of Transmembrane Regions, Cholesterol, and Ganglioside Binding Sites in Amyloid-Forming Proteins Indicate Potential for Amyloid Pore Formation.Frontiers in molecular neuroscience · 2021Article
- Article
- Increased inflammation in BA21 brain tissue from African Americans with Alzheimer's disease.Metabolic brain disease · 2020Article
- Unbiased Proteomic Approach Identifies Unique and Coincidental Plasma Biomarkers in Repetitive mTBI and AD Pathogenesis.Frontiers in aging neuroscience · 2018Article
- Intermediate and low abundant protein analysis of vitamin D deficient obese and non-obese subjects by MALDI-profiling.Scientific reports · 2017Article
- Impact of Cytokines and Chemokines on Alzheimer's Disease Neuropathological Hallmarks.Current Alzheimer research · 2017Review
- Folic acid inhibits tau phosphorylation through regulation of PP2A methylation in SH-SY5Y cells.The journal of nutrition, health & aging · 2015Article
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Authors and funding
4 authors.
Funding
Abstract
The association of inflammatory proteins with neuritic plaques in the brains of Alzheimer's disease (AD) patients has led to the hypothesis that inflammation plays a pivotal role in the development of pathology in AD. Earlier studies have shown that alpha 1-antichymotrypsin (ACT) enhances amyloid beta fibrillization and accelerated plaque formation in APP transgenic mice. Later studies from our laboratory have shown that purified ACT induces tau hyperphosphorylation and degeneration in neurons. In order to understand the mechanisms by which inflammatory proteins enhance tau hyperphosphorylation, we injected interleukin-1 β (IL-1 β ) intracerebroventricularly into mice expressing human ACT, human tau, or both transgenes. It was found that the hyperphosphorylation of tau in ACT and ACT/htau mice after IL-1 β injection correlated with increased phosphorylation of c-Jun N-terminal kinase (JNK). We verified the involvement of JNK in ACT-induced tau phosphorylation by utilizing JNK inhibitors in cultured primary neurons treated with ACT, and we found that the inhibitor showed complete prevention of ACT-induced tau phosphorylation. These results indicate that JNK is one of the major kinases involved in the ACT-mediated tau hyperphosphorylation and suggest that inhibitors of this kinase may protect against inflammation-induced tau hyperphosphorylation and neurodegeneration associated with AD.
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Registered trials
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