Publications by authors named "Nadine Rischert"
One of the pathological hallmarks of Huntington disease (HD) is accumulation of the disease-causing mutant huntingtin (mHTT), which leads to the disruption of a variety of cellular functions, ultimately resulting in cell death. Induction of autophagy, for example by the inhibition of mechanistic target of rapamycin (mTOR) signaling, has been shown to reduce HTT levels and aggregates. While rapalogs like rapamycin allosterically inhibit the mTOR complex 1 (TORC1), ATP-competitive mTOR inhibitors suppress activities of TORC1 and TORC2 and have been shown to be more efficient in inducing autophagy and reducing protein levels and aggregates than rapalogs.
View Article and Find Full Text PDFArticle Synopsis
- Huntington disease is a deadly brain disorder caused by a genetic mutation in the huntingtin protein, leading to cell dysfunction, especially in striatal neurons.
- Researchers often use STHdh cell lines from mice to study Huntington disease, but these lines show significant differences in size, growth rates, and chromosome numbers depending on whether they are wild type or mutant.
- These variances can affect research findings and interpretations, suggesting that scientists need to be careful in their experimental approaches to avoid misleading conclusions.