Price | 9275€+ |
Organism | Human |
Product Type | iPS-derived organoid |
Tissue | Brain (Midbrain) |
Disease | – |
Applications
Toxicity
Organoid Based
Disease Modeling
Brain & CNS Disease Model
With the global rise of K-beauty, the cosmetics industry continues to grow steadily. Since the ban on animal testing for cosmetics in Korea in 2017, various alternative testing methods have...
Traditional microscopy methods often require fluorescent labeling to analyze cellular structures, which can be time-consuming and invasive. In contrast, our HT-X1 system allows for high-resolution visualization of cellular morphology without...
Traditional protein analysis has primarily focused on quantifying expression levels within tissue samples. However, recent advances in spatial analysis techniques have shifted attention toward evaluating not only expression levels, but...
We conducted a study focused on identifying disease-related markers using patient-derived tissue samples. However, traditional methods limited our ability to analyze multiple candidate markers simultaneously, and the limited availability of...
Our hPSC-derived human midbrain organoids can be cultured long-term using our proprietary differentiation technology and contain more mature and larger numbers of dopamine neurons.
Our midbrain organoids have the genes and structural characteristics expressed in the human midbrain and are composed of a large number of dopamine neurons as well as various cells. When cultured for a long period of time, melanin in the substantia nigra that appears specifically in the midbrain can be observed.
In our brain organoids, electrical signals from nerve cells, characteristic of the human brain, were detected.
Through this, it was confirmed that it is a functionally mature organoid, and through long-term culture, the brain waves that appear in premature babies can also be confirmed.
We can generate organoid models of neurodegenerative diseases through two methods.
The first method is to differentiate induced pluripotent stem cells into brain organoids and create a disease model by producing GBM cells and assembloids.
The second method is to destroy or overexpress the gene to be identified in normal induced pluripotent stem cells, differentiate them into organoids, and then create a disease model.
We compared normal organoids to organoids from a Parkinson’s disease model.
Abnormal mitochondria were observed in the Parkinson’s disease model, and it was confirmed that there were fewer dopamine neurons in this organoid compared to normal organoids.
When the treatment candidate drug was treated with Parkinson’s disease organoids, it was confirmed that death of dopamine neurons was suppressed and abnormal mitochondrial function was restored.
In addition, ROS was confirmed to be reduced, so the organoid could be used to screen candidate drugs for Parkinson’s disease.
