ArticleMolecular neurobiology2015
Neuroinflammatory and Amyloidogenic Activities of IL-32β in Alzheimer's Disease.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Effect of Metformin on Plasma and Cerebrospinal Fluid Biomarkers in Non-Diabetic Older Adults with Mild Cognitive Impairment Related to Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Trial
- A peripheral proteomic signature of Alzheimer's disease is identified in the plasma extracellular vesicles of mild cognitive impairment patients from a memory clinic: the BIOPEXAL study.Research square · 2025Article
- Inflammatory Blood Biomarkers Are Associated with Long-Term Clinical Disease Severity in Parkinson's Disease.International journal of molecular sciences · 2023Article
- Placenta-derived IL-32β activates neutrophils to promote preeclampsia development.Cellular & molecular immunology · 2021Article
- The Impact of Systemic Inflammation on Alzheimer's Disease Pathology.Frontiers in immunology · 2021Review
- Interleukin 32 Promotes Foxp3Frontiers in cell and developmental biology · 2021Article
- Prevention of multiple system atrophy using human bone marrow-derived mesenchymal stem cells by reducing polyamine and cholesterol-induced neural damages.Stem cell research & therapy · 2020Article
- Plasmon-Activated Water Reduces Amyloid Burden and Improves Memory in Animals with Alzheimer's Disease.Scientific reports · 2019Article
- Article
- Role of interleukin-32 in cancer biology.Oncology letters · 2018Review
- Involvement of Astrocytes in Alzheimer's Disease from a Neuroinflammatory and Oxidative Stress Perspective.Frontiers in molecular neuroscience · 2017Review
- Toxin-Induced Experimental Models of Learning and Memory Impairment.International journal of molecular sciences · 2016Review
- Cytokines and Cytokine Receptors Involved in the Pathogenesis of Alzheimer's Disease.Journal of clinical & cellular immunology · 2016Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-32β can act as either pro-inflammatory or anti-inflammatory cytokines with being dependent on the status of disease development. Herein, we investigated whether IL-32β overexpression changes cytokine levels and affects amyloid-beta (Aβ)-induced pro-inflammation in the brain. IL-32β transgenic (Tg) mice and non-Tg mice were intracerebroventricularly infused with Aβ1-42 once a day for 14 days, and then cognitive function was assessed by the Morris water maze test and passive avoidance test. Our data showed that IL-32β Tg mice increased memory impairment, glia activation, amyloidogenesis, and neuroinflammation. The expression of glial fibrillary acid protein (GFAP), Iba1, and β-secretase 1 (BACE1) in the cortex and hippocampus was much higher in the Aβ1-42-infused IL-32β Tg mice brain. The activation of signal transducer and activator of transcription 3 (STAT3) and nuclear factor-kappa B (NF-κB) was much higher in Aβ1-42-infused IL-32β Tg mice brain. We also found that cytokines including IP-10, GM-CSF, JE, IL-13, and interferone-inducible T cell α chemoattractant (I-TAC) were elevated in Aβ1-42-infused IL-32β Tg mice brain. These results suggest that IL-32β could activate NF-κB and STAT3, and thus affect neuroinflammation as well as amyloidogenesis, leading to worsening memory impairment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.