ArticleMolecular neurobiology2025
17β-Trenbolone Increases the Release of Lipocalin 2 via the Brain-Liver Axis and Causes Alzheimer's Disease-Like Symptoms in CSDS-Induced Mice.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- The Immune-Chemokine Axis in Alzheimer's Disease: Roles of Adaptive Immune System in Neuroinflammation and Disease Progression.Biomolecules · 2026Review
- The Trenbolo(g)ne Sandwich: An International Study Comparing Health Harms Among Men Who Use Anabolic-Androgenic Steroids With and Without Trenbolone.Drug and alcohol review · 2026Article
- Down-regulation of lipocalin-2 alleviates depressive-like behaviors in mice through modulation of microglial activation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
aimsThis study aimed to investigate the neurological and behavioural effects of exposure to the environmental endocrine disruptor 17β-trenbolone (17-TB) exposure in chronic social defeat stress (CSDS)-induced mice and elucidate the role of lipocalin 2 (LCN2) in linking peripheral inflammation to neurodegeneration. METHODS AND MATERIALS: Male BALB/c mice were subjected to the CSDS paradigm and treated with 17-TB (100 μg/kg) or vehicle control for 10 consecutive days. Behavioural assessments, including novel object recognition test, novel object location test and social interaction test, were conducted to evaluate cognitive memory and social behaviour. Western blotting, ELISA and immunofluorescence were used to analyse LCN2 expression and related inflammatory markers in the liver and brain.
resultsThe results showed that 17-TB exposure exacerbated the induction of serum TNF-α and IL-1β inflammation in CSDS-induced mice, leading to activation of the hepatic IL-6 inflammatory factor pathway. This enhanced the release of hepatic LCN2 and stimulated its expression in the medial prefrontal cortex (mPFC) via the peripheral circulation, which subsequently activated the dorsal motor vagal nucleus (DMX) through cholinergic neuron (ChAT
conclusionThis study highlights the critical role of the brain-liver axis in inducing LCN2 release and ultimately cognitive deficits similar to AD-like symptoms in a 17-TB-exposed CSDS-induced mouse model, highlighting the risk of environmental endocrine disruptors causing neurodegenerative diseases that require further investigations and safety assessments.
Indexed as
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40622522What OpenQuestion holds
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.