Scientists have discovered a signalling pathway alteration in embryos with Huntington’s disease, paving the way for ground-breaking treatments.
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Researchers have reported that nano-micelles can be used to efficiently deliver CRISPR-Cas9 to edit genes in the brains of mice.
Using NMR spectroscopy, researchers have partially observed the structure of heat shock proteins that bind to proteins that cause Huntington's disease.
Researchers have found the TBK1 enzyme regulates the degradation and clearance of the huntingtin protein, making it a drug target for Huntington's disease.
Researchers show that the mutated huntingtin protein associated with Huntington’s disrupts the transport of essential proteins within the neuron, potentially highlighting an early cause of the disease.
By administering a one-time PTB antisense oligonucleotide therapy to mice, researchers observed an increase in neurons and elimination of Parkinson's from the models.
Two studies reveal the importance of timing in Huntington’s disease interventions and demonstrate interleukin-6 may play a protective role.
A group of researchers has synthesised a new class of ligands which bind with high affinity to imidazoline I2 receptors, a drug target for Alzheimer's disease.
Researchers have developed a new regenerative gene therapy using neurogenic differentiation, which has shown efficacy treating Huntington's disease in mice.
Researchers show Naphthyridine-Azaquinolone (NA) could be a possible future therapy able to slow the progression and improve the symptoms of Huntington’s disease.
Researchers have conducted a genetic screen in mice to discover a family of genes that contributes to the development of Huntington's.
Scientists have evaluated mouse models used for developing treatments for mood disorders associated with Huntington's disease and have recommended which have greater potential for success.