Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.mehy.2020.110065 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
A supercritical oil extract of seeds ameliorates Huntington's disease-like symptoms and neuropathology: the potential role of anti-oxidant and anti-inflammatory effects.
Front Pharmacol
December 2024
Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Background: Huntington disease (HD), a neurodegenerative autosomal dominant disorder, is characterized by involuntary choreatic movements with cognitive and behavioral disturbances. Up to now, no therapeutic strategies are available to completely ameliorate the progression of HD. has various pharmacologic effects such as antioxidant and anti-inflammatory activities.
View Article and Find Full Text PDFHuntington's Disease (HD), a progressive neurodegenerative disorder with no disease-modifying therapies, is caused by a CAG repeat expansion in the HD gene encoding polyglutamine-expanded huntingtin (HTT) protein. Mechanisms of HD cellular pathogenesis and cellular functions of the normal and mutant HTT proteins are still not completely understood. HTT protein has numerous interaction partners, and it likely provides a scaffold for assembly of multiprotein complexes many of which may be altered in HD.
View Article and Find Full Text PDFAnti-gene oligonucleotide clamps invade dsDNA and downregulate expression.
Mol Ther Nucleic Acids
December 2024
Department of Laboratory Medicine, Karolinska Institutet, ANA Futura, Alfred Nobels Allé 8, 14152 Huddinge, Stockholm, Sweden.
Anti-gene oligonucleotides belong to a group of therapeutic compounds, which, in contrast to antisense oligonucleotides, bind to DNA. Clamp anti-gene oligonucleotides bind through a double-stranded invasion mechanism. With two arms connected by a linker, they hybridize to one of the DNA strands forming Watson-Crick and Hoogsteen hydrogen bonds.
View Article and Find Full Text PDFAberrant splicing in Huntington's disease accompanies disrupted TDP-43 activity and altered m6A RNA modification.
Nat Neurosci
January 2025
Department of Neurobiology & Behavior, University of California, Irvine, Irvine, CA, USA.
Huntington's disease (HD) is caused by a CAG repeat expansion in the HTT gene, leading to altered gene expression. However, the mechanisms leading to disrupted RNA processing in HD remain unclear. Here we identify TDP-43 and the N6-methyladenosine (m6A) writer protein METTL3 to be upstream regulators of exon skipping in multiple HD systems.
View Article and Find Full Text PDFAssociation of real life postural transitions kinematics with fatigue in neurodegenerative and immune diseases.
NPJ Digit Med
January 2025
Department of Neurology, University Hospital Schleswig-Holstein Campus Kiel, Kiel University, Kiel, Germany.
Fatigue is prevalent in immune-mediated inflammatory and neurodegenerative diseases, yet its assessment relies largely on patient-reported outcomes, which capture perception but not fluctuations over time. Wearable sensors, like inertial measurement units (IMUs), offer a way to monitor daily activities and evaluate functional capacity. This study investigates the relationship between sit-to-stand and stand-to-sit transitions and self-reported physical and mental fatigue in participants with Parkinson's, Huntington's, rheumatoid arthritis, systemic lupus erythematosus, primary Sjögren's syndrome and inflammatory bowel disease.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!