Researchers discovered decreased function in a protein critical for synaptic function in those with Huntington's disease.
Converting skin cell samples into neurons helps researchers gain a better understanding of the mechanisms of Huntington's disease.
Researchers have created a comprehensive atlas of cell types in the brain's cerebrovascular system.
A new study sheds light on the genetic causes of a range of neurodegenerative disorders, including ALS, Parkinson's disease, and Huntington's disease, and determines factors that impact the age of onset as well as disease severity.
Synthesizing a human embryo from stem cells and using gene editing to insert the Huntingtin gene, researchers found the mutation affected the size of germ layers compared to the control embryos. Findings suggest Huntington's disease may be a neurodevelopmental disorder that presents as a neurodegenerative disease later
Disruption of autophagy may be at the root of the cognitive deficits experienced by those with Huntington's disease.
The mutated huntingtin protein slows ribosome movement and decreases protein synthesis.
A new study adds to the growing body of evidence that the origin of Huntington's disease is rooted in childhood. Researchers say the HTT gene mutation affects both brain and body growth during development, and the increased susceptibility of brain cell death begins early in life.
Researchers find a previously unknown connection between ALS, FTD, and the Huntington's disease associated gene, huntingtin.
Study provides evidence of gut dysbiosis associated with Huntington's disease. Some of the gut measures were associated with disease symptoms such as movement and cognitive impairment. The findings could provide a new avenue of treatment for the neurodegenerative disease.
In both human cell and mouse models of Huntington's disease, RNA from mitochondria was misplaced within spiny projection neurons. The stray RNAs, which looked different to cells than RNA derived from the cell nucleus, trigger an immune reaction that can lead to striatal cell type vulnerability.
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.
