The mutated huntingtin protein slows ribosome movement and decreases protein synthesis.
A mutated form of the huntingtin protein disrupts the normal movement of vesicles holding HT and Rab4. This leads to defects in synapses, resulting in movement abnormalities and lifespan decreases in fruit fly larvae. Findings suggest Rab4 could be a novel therapeutic target for the early intervention of Huntington's disease, before the neuronal loss and behavioral deficits associated with the neurodegenerative disorder.
Mouse models of corticospinal injuries reveal adult neurons begin a natural regeneration process by reverting back to an embryonic state. The regeneration is sustained with the help of a gene more commonly associated with Huntington's disease.
Researchers say the Huntingtin gene affects brain development from an early age, even though most patients do not develop Huntington's disease until later life.
Researchers have identified a mechanism that may reduce the toxic aggregation of the huntingtin protein. The findings could lead to new treatment options for Huntington's patients.
Researchers have decoded the 3D structure of the Huntingtin protein. The discovery may help develop new treatments for Huntington's disease.
Rockefeller University researchers reveal Huntington's neurons are much larger than healthy cells.
A new study reveals a new molecular mechanism for Huntington's disease.
Researchers have identified a protein that can turn off the Huntingtin gene's expression.
Researchers improve motor function and reduce brain shrinkage in animal models of HD by adjusting the levels of a signaling protein.
The Htt protein, which is mutated in Huntington's disease patients, is critical for wiring the brain in early life, a new study reports.
Researchers work to understand how expanded polyglutamine tracts form the types of supramolecular structures that are presumed to be toxic to neurons.
