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c9orf72-ftd
3 studies tagged c9orf72-ftd, dated 2014-05-09 to 2023-11-29. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- G2C4 targeting antisense oligonucleotides potently mitigate TDP-43 dysfunction in human C9orf72 ALS/FTD induced pluripotent stem cell derived neurons 2023-11-29
- Poly(GR) and poly(GA) in cerebrospinal fluid as potential biomarkers for C9ORF72-ALS/FTD 2022-05-19
- Antisense oligonucleotide therapy for the treatment of C9ORF72 ALS/FTD diseases 2014-05-09
Studies
3 studies carry this tag.
Date range
2014 to 2023
Top journals
- Acta neuropathologica 1
- Molecular neurobiology 1
- Nature communications 1
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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The G 4 C 2 repeat expansion in the C9orf72 gene is the most common genetic cause of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.
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GGGGCC repeat expansion in C9ORF72, which can be translated in both sense and antisense directions into five dipeptide repeat (DPR) proteins, including poly(GP), poly(GR), and poly(GA), is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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Motor neuron disorders, and particularly amyotrophic lateral sclerosis (ALS), are fatal diseases that are due to the loss of motor neurons in the brain and spinal cord, with progressive paralysis and premature death.