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.
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.
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.
Study reports it may be possible to detect the onset and progression of Huntington's disease through linguistic changes in patients. Linguistic impairments often begin before the onset of other Huntington's symptoms.
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Combining artificial intelligence technology and blood samples, researchers were able to predict and explain the progression of Alzheimer's and Huntington's disease. The new algorithm was able to detect alterations in gene expression over decades from patients' blood samples.
Using induced pluripotent stem cells derived from patients with neurodegenerative disorders, researcher recreated the blood-brain barrier inside Organ-Chips.
Genetic mutations which lead to abnormal RNA in regions of repeat DNA sequences set off anti-viral like inflammatory responses. This leads to apoptosis and ultimately trigger the onset of neurodegenerative diseases.