Price | 9275€+ Login to see price |
Organism | Human |
Product Type | iPS-derived organoid |
Tissue | Brain (Midbrain) |
Disease | – |
Applications
Toxicity
Organoid Based
Disease Modeling
Brain & CNS Disease Model
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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.
FOXA2 – A transcription factor crucial for the development and differentiation of midbrain and hindbrain neurons, promoting the formation of midbrain dopaminergic neurons.
LMX1A – A transcription factor that regulates the differentiation of dopaminergic neurons in the midbrain and hindbrain.
TH (Tyrosine Hydroxylase) – An enzyme involved in dopamine synthesis, commonly used as a marker for dopaminergic neurons.
Nestin – A marker for neural progenitor cells and immature neurons, indicating immature cells in midbrain organoids.
OTX2 – A transcription factor important for the development of the forebrain and midbrain, expressed in the midbrain and brainstem regions.
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: creating brain disease organoids using iPSCs with regulated expression of specific genes or inducing brain disease organoids through drug treatment.
Two main approaches are used to model Parkinson’s disease. The first involves utilizing gene editing technologies to modify or alter genes associated with Parkinson’s, such as introducing mutations in LRRK2 or SNCA to replicate disease-causing genes and analyze pathological features. The second approach involves creating organoids from patient-derived iPSCs (induced pluripotent stem cells). By using iPSCs from Parkinson’s patients, personalized disease models can be developed, allowing researchers to experimentally recreate disease characteristics like dopaminergic neuronal degeneration and study drug development and therapeutic strategies.
Parkinson’s disease is a neurodegenerative disorder characterized by the progressive loss of dopamine-producing neurons, with mitochondrial dysfunction playing a significant role in its pathology. Mitochondrial swelling, the abnormal enlargement of mitochondria, is a key process involved in the onset and progression of Parkinson’s disease. This swelling disrupts energy production and calcium homeostasis, ultimately leading to cell death. Additionally, mitochondrial dysfunction increases oxidative stress and disrupts intracellular signaling, contributing to the damage of dopamine neurons and the motor symptoms of Parkinson’s disease, such as tremors and movement impairments.
The experiment comparing the expression of th (tyrosine hydroxylase) and ccasp3 (cleaved caspase-3) after treatment with CCCP (a mitochondrial toxin) in Parkinson’s disease organoids is crucial for studying mitochondrial dysfunction and cell death mechanisms.
CCCP depolarizes the mitochondrial membrane potential, inhibiting mitochondrial function and inducing damage to dopamine-producing neurons. In the experiment, th serves as a marker for dopamine-producing neurons, while ccasp3 is a marker for apoptosis.
The results showed a decrease in th expression and an increase in ccasp3 expression following CCCP treatment. This suggests that mitochondrial dysfunction induced by CCCP leads to damage to dopamine neurons and enhances cell death. These findings help confirm the link between mitochondrial dysfunction and cell death pathways in Parkinson’s disease and may offer valuable insights for developing new therapeutic approaches.
This compound selectively binds to superoxide, a major marker of oxidative stress produced in the mitochondria. After CCCP treatment, the expression of MitoSOX was increased, indicating an elevation in mitochondrial oxidative stress. This supports the notion that mitochondrial dysfunction plays a critical role in Parkinson’s disease.
JC-1 is used to measure mitochondrial membrane potential. When mitochondria are healthy, JC-1 shifts from green to red fluorescence, while a decrease in membrane potential causes a shift from red to green. After CCCP treatment, there was a tendency for JC-1 expression to shift from red to green, indicating a depolarization of the mitochondrial membrane and loss of function.
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info@lambdabiologics.com
