Ace Therapeutics is dedicated to helping researchers and professionals understand the biology associated with mental illness, explore new therapies and strategies for mental illness, and develop new biomarkers for mental illness. We aim to provide biologically relevant and predictive cellular models to provide unparalleled insight into cellular behavior, thereby significantly advancing bipolar disorder research and drug discovery.

Introduction of Cellular Model Development for Bipolar Disorder

Bipolar disorder (BD) is a chronic, severe psychiatric disorder that imposes a heavy health burden worldwide. Understanding the in vitro cellular network of BD patients may allow us to understand the interface between genetic variation and susceptibility and response to treatment in BD. Cellular modeling has proven useful in BD and potential pathways have been identified, particularly in cellular resilience-related mechanisms. At the cellular level, cell-based models can be used to measure spontaneous and stimulated patterns of neuronal network activity. In addition, using cell-based models, BD can be studied by observing the abnormal development of neurons and their circuits in vitro.

Fig. 1 A true understanding of PD must encompass different systems at different physiological levels: molecular, cellular, and behavioral. (Schloesser RJ, et al., 2008)

Cellular Model Development Services for Bipolar Disorder

Ace Therapeutics offers 2 main cell culture systems for pathophysiological studies of BD and drug development for the anti-bipolar disorder, respectively non-neuronal and neuronal cell lines. Our non-neuronal models include mainly lymphoblastoid cell lines and fibroblasts. In non-neuronal cell models, we can help you discover abnormalities in genes including calcium signaling, endoplasmic reticulum stress response, mitochondrial oxidative pathways, membrane ion channels, circadian system, and apoptosis-related genes. These processes are critical for cellular dynamic homeostasis, plasticity, signal transduction, and cell survival.

Our neuronal cell model consists mainly of the olfactory neuronal epithelium (ONE) and neurons reprogrammed from induced pluripotent stem cells (IPSC). The analysis of genes related to inositol metabolism, apoptosis, catecholamine metabolism, and protein biosynthesis based on neuronal cell models helps to understand the pathogenesis of BD. I can differentiate IPSCs into cortical glutamatergic and GABAergic neuronal populations, midbrain dopaminergic neuronal populations, or hippocampal neurons, depending on your research needs. In addition, we offer neuro-analysis services based on iPSC-derived neurons. We generate new insights into the mechanisms underlying the onset, development, and eventual treatment of BD by generalizing and monitoring health and disease networks in culture dishes.

Cellular Model-based Neuronal Analysis Services

We provide high-content imaging of neurons for characterizing and measuring changes in neuronal networks, such as axon number, length and branching, as well as determining overall or specific toxic responses. We use automated microscopy and high-content analysis software to quickly and accurately capture and quantify neuronal activity.

• Neuronal growth analysis
• Neuronal morphology analysis
• Neurotoxicity analysis
• Phenotypic screening of iPSC-derived neurons

Ace Therapeutics aims to help you develop new strategies for psychotropic drug discovery. We address current limitations by identifying disease-related functional responses in a variety of patient-derived cells, such as iPSC-derived neurons and organoid or peripheral blood mononuclear cells. These models facilitate robust and rapid network analysis of BD neurons. We aim to help you discover molecular targets for drug discovery and potential new drugs in drug screening. If you are interested in this service please make an inquiry to learn how we can support you in your project.

Reference

1. Schloesser RJ, Huang J, Klein PS, Manji HK. Cellular plasticity cascades in the pathophysiology and treatment of bipolar disorder. Neuropsychopharmacology. 2008, 33(1):110-133.