A new study led by the University of California, Irvine found that markers of chronic cellular stress previously associated with neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) persisted. It was found that it also occurs in the brain of Huntington’s disease. Illness (HD) patients.
Chronic cell stress results in the abnormal accumulation of stress granules (SG), which are clumps of proteins and RNA that collect inside cells. Before this study Clinical Research JournalIt was unclear whether these types of granules were a pathological feature of HD. It is a hereditary, progressive neurodegenerative disease that usually occurs at the height of life.
In addition to identifying SG as a pathological feature of HD, researchers have found that extracellular vesicles, which float in the cerebrospinal fluid (CSF) and act as a messaging system between cells in the brain, behave like other cells. Some other discoveries, including the potential to alter, affect the abnormal accumulation of granules.
They also found that TAR DNA-binding protein 43 (TDP43) was mislocalized. It has emerged as an important feature of multiple neurodegenerative diseases.
We were initially interested in whether these message profiles could serve as biomarkers for HD, and whether they contained messages that differed from the vesicles of individuals who were not affected by the vesicles of HD patients. I investigated. “
Isabella I. Sanchez, PhD, Lead Author of Research, Thompson Institute, UCI School of Medicine
Researchers have found that CSF in HD patients carries the message in the form of small non-coding RNAs (miRNAs) that are predicted to alter the production of proteins essential for SG formation. They quickly identified GTPase-activating protein-binding protein 1 (G3BP1), a major player in SG dynamics, as a predicted target.
“This discovery of miRNAs was very exciting because we started a study that characterizes SG in HD brain tissue at the same time. It can be very difficult to detect SG in brain tissue, just by chance with the right conditions. We’ve narrowed it down. We’re ready to characterize G3BP1SG in the brains of HD mice and HD patients, “said Dr. Leslie M. Thompson, Donald Bren, and UCI’s undergraduate professor. Psychiatry & UCI School of Medicine Human Behavior and Biochemistry, and UCI School of Biological Sciences Neurobiology and Behavior.
SG formation is a normal physiological process that allows cells to overcome stressful conditions, but SG pathology in HD initially served a protective function, but over time it evolved into a hyperstable structure G3BP1SG May be due to the accumulation of.
“Our findings understand how SG accumulation affects the progression of HD, and whether targeting SG pathology is a viable therapeutic tool in the fight against HD. I hope it will be useful for future research aimed at. ”He is also the lead author of the research.
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