ArticleInternational journal of molecular sciences2023
T1AM/TAAR1 System Reduces Inflammatory Response and β-Amyloid Toxicity in Human Microglial HMC3 Cell Line.
Article in International journal of molecular sciences, 2023. 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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21 citing papers in PubMed, 25 citations in OpenAlex.
- Effect of MALT1 inhibition by MI‑2 on the microglial phenotype switch, inflammatory cytokine secretion, neuronal loss and oxidative stress in Alzheimer's disease.International journal of molecular medicine · 2026Article
- Novel Insights into the Pleiotropic Neuroprotective Action of Synthetic Halogen Free Thyronamine-like Analogues.Molecules (Basel, Switzerland) · 2026Article
- From Stress to Neurodegeneration: A New Look at the Pathogenesis of Parkinson's Disease.Biomedicines · 2026Review
- The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026Review
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- Global research trends on thyroid hormones and neurodegenerative diseases: a bibliometric study from 2015 to 2025.Frontiers in aging neuroscience · 2026Article
- Calcium at the crossroads of the immunometabolic signaling and comorbidity in schizophrenia.Frontiers in synaptic neuroscience · 2026Article
- The Role of Thyroid Hormones in Neurodegenerative Disorders: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Role of Glial Trace Amine Associated Receptor 1 (TAAR1) and Microbiota in Schizophrenia.Neurochemical research · 2025Review
- Transcriptomic Analysis ofBrain sciences · 2025Article
- Thyroid hormone signaling in ocular development and diseases.Biological research · 2025Review
- Multi-Target Protective Effects of β-Caryophyllene (BCP) at the Intersection of Neuroinflammation and Neurodegeneration.International journal of molecular sciences · 2025Article
- Modulating autism spectrum disorder pathophysiology using a trace amine-focused approach: targeting the gut.Molecular medicine (Cambridge, Mass.) · 2025Review
- Trace amine-associated receptor 1 (TAAR1): an emerging therapeutic target for neurodegenerative, neurodevelopmental, and neurotraumatic disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Article
- Article
- Trace Amine-Associated Receptors' Role in Immune System Functions.Biomedicines · 2024Review
- Discovery of a Novel Chemo-Type for TAAR1 Agonism via Molecular Modeling.Molecules (Basel, Switzerland) · 2024Article
- Article
- Discovery of Guanfacine as a Novel TAAR1 Agonist: A Combination Strategy through Molecular Modeling Studies and Biological Assays.Pharmaceuticals (Basel, Switzerland) · 2023Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglial dysfunction is one of the hallmarks and leading causes of common neurodegenerative diseases (NDDs), including Alzheimer's disease (AD) and Parkinson's disease (PD). All these pathologies are characterized by aberrant aggregation of disease-causing proteins in the brain, which can directly activate microglia, trigger microglia-mediated neuroinflammation, and increase oxidative stress. Inhibition of glial activation may represent a therapeutic target to alleviate neurodegeneration. Recently, 3-iodothyronamine (T1AM), an endogenous derivative of thyroid hormone (TH) able to interact directly with a specific GPCR known as trace amine-associated receptor 1 (TAAR1), gained interest for its ability to promote neuroprotection in several models. Nevertheless, T1AM's effects on microglial disfunction remain still elusive. In the present work we investigated whether T1AM could inhibit the inflammatory response of human HMC3 microglial cells to LPS/TNFα or β-amyloid peptide 25-35 (Aβ25-35) stimuli. The results of ELISA and qPCR assays revealed that T1AM was able to reduce microglia-mediated inflammatory response by inhibiting the release of proinflammatory factors, including IL-6, TNFα, NF-kB, MCP1, and MIP1, while promoting the release of anti-inflammatory mediators, such as IL-10. Notably, T1AM anti-inflammatory action in HMC3 cells turned out to be a TAAR1-mediated response, further increasing the relevance of the T1AM/TAAR1 system in the management of NDDs.
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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.