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Cracking the cryptic code in amyotrophic lateral sclerosis and frontotemporal dementia: Towards therapeutic targets and biomarkers

1 May 2022

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two devastating human neurodegenerative diseases. A hallmark pathological feature of both diseases is the depletion of the RNA-binding protein TDP-43 from the nucleus in the brain and spinal cord of patients. A major function of TDP-43 is to repress the inclusion of cryptic exons during RNA splicing. When it becomes depleted from the...

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PMID: 35567447
DOI: 10.1002/ctm2.818

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Cracking the cryptic code in amyotrophic lateral sclerosis and frontotemporal dementia: Towards therapeutic targets and biomarkersPMID 35567447Read ↗

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TDP-43 represses cryptic exon inclusion in FTD/ALS gene <i>UNC13A</i>Semantic proximity Read ↗

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TDP-43 and other hnRNPs regulate cryptic exon inclusion of a key ALS/FTD risk gene, UNC13ASemantic proximity Read ↗

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Quantitative analysis of cryptic splicing associated with TDP-43 depletionSemantic proximity Read ↗

Common ALS/FTD risk variants in UNC13A exacerbate its cryptic splicing and loss upon TDP-43 mislocalizationSemantic proximity Read ↗

Common ALS/FTD risk variants in <i>UNC13A</i> exacerbate its cryptic splicing and loss upon TDP-43 mislocalizationSemantic proximity Read ↗

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Inhibition of nonsense-mediated decay in TDP-43 deficient neurons reveals novel cryptic exonsSemantic proximity Read ↗

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