ArticleTrends in genetics : TIG2022
Cryptic inclusions UNCover losses driving neurodegeneration.
Article in Trends in genetics : TIG, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Engram cell vulnerability in neurodegeneration: from mechanistic insights to therapeutic horizons.Frontiers in aging neuroscience · 2026Review
- Synaptic changes contribute to persistent extra-motor behaviour deficits in amyotrophic lateral sclerosis.Acta neuropathologica communications · 2025Article
- Molecular mechanisms and consequences of TDP-43 phosphorylation in neurodegeneration.Molecular neurodegeneration · 2025Review
- Unlocking Disease-Modifying Treatments for TDP-43-Mediated Neurodegeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- A transient protein folding response targets aggregation in the early phase of TDP-43-mediated neurodegeneration.Nature communications · 2024Article
- Review
- DPPA5A suppresses the mutagenic TLS and MMEJ pathways by modulating the cryptic splicing ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Aggregation-prone TDP-43 sequesters and drives pathological transitions of free nuclear TDP-43.Cellular and molecular life sciences : CMLS · 2023Article
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2 authors.
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Abstract
Pathology formed by the protein TDP-43 (TAR DNA binding protein 43) is the hallmark of several neurodegenerative diseases. Recent studies by Ma et al. and Brown et al. reveal that loss of TDP-43 function causes inclusion of cryptic exons in specific mRNAs, including the synaptic gene UNC13A, a known genetic risk factor for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). These findings suggest new disease mechanisms.
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