Recently, a research report titled “An ancient polymorphic regulatory region within the BDNF gene associated with obesity modulates anxiety-like behavior in mice and humans” was published in the journal Molecular Psychology. Scientists from institutions such as the University of Aberdeen found through their research that special DNA regions in the human genome may play an important role in controlling anxiety disorders in the body, this key gene may affect the anxiety level of the mouse body.
According to data from the Mental Health Foundation, after the COVID-19 pandemic, the proportion of anxiety patients is constantly increasing, with up to one-fifth of people experiencing anxiety most or all of the time. Moreover, reports have shown that one-third of patients taking anti-anxiety drugs did not receive sustained anxiety relief. Researchers hope that further research on this switch can help improve the lives of anxiety patients by identifying new drug targets.
Researcher Mackenzie explained that they already know that 95% of genetic differences associated with diseases are found outside of protein-coding genes, which are called non-coding genomes and have not yet been well studied. Therefore, we lack the tools to conduct in-depth research on them.
Researchers suggest that non-coding genomes contain information in the form of gene switches, which may tell genes when and where they are turned on, which is crucial because genes must be turned on in the right cells and at the right time to ensure overall health. And when it is not properly turned on, it can cause diseases such as anxiety, depression, and addiction, which are the regions of the non-coding genome that researchers are studying in the laboratory.
Researchers have found that the approach to understanding the crucial role of non-coding genomes in anxiety, addiction, and obesity is unique. Today, researchers realize that many of these switches remain unchanged or have been preserved for billions of years, and this can be found in both mice and human bodies.
Our Featured Products
| Cat. No. | Product Name | Source (Host) | Species | Tag |
| BDNF-243H | Recombinant Human BDNF protein, His-tagged | E.coli | Human | His |
| BDNF-10202H | Recombinant Human BDNF, GST-tagged | E.coli | Human | GST |
| BDNF-022H | Active Recombinant Human Brain-Derived Neurotrophic Factor | E.coli | Human | N/A |
| BDNF-01HG | Active GMP Recombinant Human BDNF Protein | CHO-K1 | Human | N/A |
The researchers used CRISPR to propose these conservative switches in the mouse body, and then studied their roles in emotions, food intake, and alcohol preference. Using CRISPR technology to eliminate specific regions in the genome, researchers focused on studying the enhancer called BE5.1, which can control the well-known BDNF gene, thereby increasing anxiety levels in female organisms. This also indicates that BE5.1 is a key part of the complex genomic mechanism in the brain that regulates anxiety.
Previously, researchers discovered other highly conserved switches that, when removed from the mouse genome, could help reduce anxiety, appetite, and alcohol intake. At the same time, researchers also provided templates to further reveal the function of enhancers in complex disease-related behaviors.
The first author of the article, Andrew McEwan, said that to understand the foundation of complex human diseases, including mental illness and other diseases such as obesity, depression, and addiction, it is equally important to understand the mechanisms of protein action in cells and the functions of proteins themselves.
Finally, the researchers suggest that only by better understanding the functions of non-coding genomes in health and disease, as well as the key roles played by thousands of mysterious gene switches lurking deep within them, may their research goals be achieved.
Related Products and Services
Protein Expression and Purification Services
Reference
McEwan, A.R., Hing, B., Erickson, J.C. et al. An ancient polymorphic regulatory region within the BDNF gene associated with obesity modulates anxiety-like behaviour in mice and humans. Mol Psychiatry (2024). doi：10.1038/s41380-023-02359-7