The Change of Noncoding RNA Expression in Olfactory Bulb of Hepatic Encephalopathy Mouse Model: Transcriptomic
Young-Kook Kim1,2, Sujung Yeom3, Seo Yoon Choi1,4
1Biomedical Science Graduate Program (BMSGP), Chonnam National University, Hwasun, Republic of Korea.
CNS Neuroscience & Therapeutics
|September 4, 2025
Summary
Hepatic encephalopathy (HE) impairs the sense of smell due to ammonia toxicity. This study reveals key RNA changes in the olfactory bulb, offering insights into HE
Area of Science:
- Neuroscience
- Biochemistry
- Genomics
Background:
- Hepatic encephalopathy (HE) is a neuropsychiatric disorder linked to cirrhosis and ammonia toxicity.
- Ammonia-induced neurotoxicity contributes to neuroinflammation and cognitive deficits in HE.
- Olfactory dysfunction is increasingly recognized as an early indicator of HE.
Purpose of the Study:
- To investigate the molecular mechanisms of HE-related olfactory dysfunction.
- To identify key RNA alterations in the olfactory bulb associated with HE.
- To compare ammonia toxicity effects in the olfactory bulb versus the cerebral cortex.
Main Methods:
- Used bile duct ligation (BDL) mice as a model for hepatic encephalopathy.
- Performed comprehensive RNA profiling (coding and noncoding RNAs) in olfactory bulbs.
- Compared transcriptomic changes between HE and high-fat diet models.
Main Results:
- Confirmed physiological alterations in olfactory cells due to ammonia.
- Identified specific coding and noncoding RNAs altered in the olfactory bulb of HE mice.
- Found common RNA changes in the olfactory bulb and cerebral cortex in HE, and across different metabolic models.
Conclusions:
- The study provides a valuable transcriptomic dataset for understanding HE-related olfactory dysfunction.
- Identified molecular signatures associated with ammonia toxicity in the olfactory system.
- Findings may guide future research into therapeutic strategies for HE.
