Huntington's disease (HD) is a hereditary neurodegenerative disorder that leads to the progressive loss of neurons, particularly in the basal ganglia, resulting in a cascade of motor, cognitive, and psychiatric symptoms. It is caused by an abnormal expression of CAG repeats in the huntingtin gene (HTT), which leads to an extended polyglutamine (polyQ) stretch in the huntingtin protein. To unravel the complexities of Huntington's disease pathogenesis and test potential therapeutic interventions, researchers use in vitro and in vivo Huntington's disease models.
Fig. 1 Different Huntington's disease models are illustrated schematically. (Rana N, et al., 2024)
At CD BioSciences, we take pride in our ability to offer customized Huntington's disease models that cater to the unique needs of aging research. Our team of seasoned experts leverages the latest scientific advances to develop innovative solutions that enable clients to understand the complexities of this debilitating neurological disorder.
The human embryonic kidney (HEK-293) cell line has been extensively utilized in Huntington's disease studies. Our scientists can customize this cell line to harbor specific Huntington's disease-causing mutations, allowing clients to investigate the cellular and molecular changes associated with the aging process in Huntington's disease pathogenesis.
We offer customized neuronal cell lines, such as motor neurons and cortical neurons. Our models can be engineered to exhibit age-dependent phenotypes, enabling clients to explore the interplay between Huntington's disease and the hallmarks of aging.
We offer tailored C. elegans models that display age-related Huntington's disease phenotypes, enabling clients to explore the molecular pathways and cellular mechanisms involved in the disease progression in an accelerated lifespan.
Our team has extensive experience in developing D. melanogaster models that exhibit age-dependent Huntington's disease-like phenotypes, such as progressive neurodegeneration, motor impairments, and cognitive deficits. Our customized models allow clients to investigate the intricate interplay between Huntington's disease pathogenesis and the aging process.
Rodents, particularly mice and rats, have long been the backbone of Huntington's disease research due to their genetic and physiological similarities to humans. At CD BioSciences, we utilize toxins including quinolinic acid (QA) and 3-nitropropionic acid (3-NP) to help clients customize animal models of Huntington's disease that exhibit key features of the disease. We also specialize in customizing transgenic and knock-in rodent models that faithfully recapitulate the hallmarks of Huntington's disease. Our scientists can modify the CAG repeats, introduce HTT mutations, or incorporate aging phenotypes to better mimic the progression of the disease in the context of aging.
| Model types | Species | Animal models |
| Transgenic models | Mouse | R6/2, R6/1, N171-82Q, YAC |
| Knock-in models | Mouse | HdhQ92, HdhQ111, CAG140, CAG15O |
CD BioSciences recognizes that understanding the intricate relationship between Huntington's disease and the aging process is crucial for developing effective therapies. Leveraging reliable techniques, we offer comprehensive analysis services to investigate the key hallmarks of aging that contribute to Huntington's disease pathogenesis, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication.
By combining our expertise in Huntington's disease model customization and in-depth analysis of aging-related processes, CD BioSciences enables clients to uncover novel insights, identify potential therapeutic targets, and accelerate the development of innovative interventions for Huntington's disease. If you are interested in our services, please feel free to contact us or make an online inquiry.
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