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Updated: May 31, 2026

A Free-breathing fMRI Method to Study Human Olfactory Function
Published on: July 30, 2017
Neurobiological mechanisms of olfactory dysfunction: a ten-year bibliometric and visualization analysis
Yuxin Zhu1,2, Yutian Chen1,2, Genki Izumoji1,2
1The Third Affiliated Hospital of Zhejiang Chinese Medical University (Zhongshan Hospital of Zhejiang Province), Hangzhou, Zhejiang, China.
Background:
Olfactory dysfunction (OD) has gained prominence in neurodegenerative diseases and COVID-19 sequelae in recent years. Its mechanisms have also attracted increasing research interest. However, there is currently a scarcity of bibliometric analyses in this field.
Methods:
Articles related to OD mechanisms were searched in the Web of Science Core Collection (WoSCC) and Scopus. Data merging and bibliometric analysis were conducted using CiteSpace, VOSviewer, Excel, Scimago Graphica, and the bibliometrix in R package. Simultaneously, PubMed was used to search and summarize interventional clinical trials in this field, and their protocols were tracked through trial registration information and ethical approval records.
Results:
A total of 7,915 articles met the inclusion criteria in WoSCC and Scopus. Overall, the number of articles published annually on the mechanisms of OD is on the rise. The USA (2635 publications), University of California System (143 publications), and Thomas Hummel (174 publications) are the most productive country, institution, and author, respectively. Keyword analysis shows that "COVID-19," "Parkinson's disease," "inflammation," "odorant receptor," and other related topics are hot topics and trends in research. PubMed retrieved and included 14 interventional clinical trials. These trials mainly focus on pharmacological interventions, non-pharmacological interventions, surgical interventions, and mechanistic studies.
Conclusion:
Mechanistic research on OD is advancing from macroscopic observations to precise molecular mechanisms. This review synthesizes evidence on how distinct etiologies, ranging from post-viral and inflammatory damage to neurodegeneration and metabolic imbalances, contribute to OD. Notably, the dysregulation of the inflammatory NF-κB, signal-transducing cAMP, and neuroregenerative Wnt/β-catenin pathways may collectively contribute to the development of OD. By integrating bibliometric trends with clinical trial evaluations, this study delineates a clear translational pipeline from mechanism exploration to clinical interventions.
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