Publications by authors named "Annesha King"
Article Synopsis
- * Research using BACHD mice and dnSNARE mice showed that reducing SNARE-dependent exocytosis protects against brain cell loss in the striatum but not in the cortex.
- * The study found changes in amino acid transporter expressions, with significant normalization of GAT3 levels when SNARE-dependent exocytosis was reduced, suggesting a potential therapeutic target in HD.
Huntington's disease (HD) is a dominantly inherited, adult-onset neurodegenerative disease characterized by motor, psychiatric, and cognitive abnormalities. Neurodegeneration is prominently observed in the striatum where GABAergic medium spiny neurons (MSN) are the most affected neuronal population. Interestingly, recent reports of pathological changes in HD patient striatal tissue have identified a significant reduction in the number of parvalbumin-expressing interneurons which becomes more robust in tissues of higher disease grade.
View Article and Find Full Text PDFHuntington's disease (HD) is a dominantly inherited neurodegenerative disease caused by a polyglutamine expansion in the widely expressed huntingtin protein. Multiple studies have indicated the importance of mutant huntingtin (mHTT) in astrocytes to HD pathogenesis. Astrocytes exhibit SNARE-dependent exocytosis and gliotransmission, which can be hampered by transgenic expression of dominant negative SNARE (dnSNARE) in these glial cells.
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- * Researchers studied the impact of CAR8, a crucial regulator in calcium signaling, on cerebellar circuits to understand diseases lacking clear neurodegeneration.
- * Their findings reveal that improper molecular development affects cerebellar wiring and activity of Purkinje cells, leading to movement issues without cell death; restoring their function can improve movement and correct circuit malformations.