Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Molecular mechanisms linking loss of TDP-43 function to amyotrophic lateral sclerosis/frontotemporal dementia-related genes.

Neuroscience research - 1 Nov 2024

Koike Yuka

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are characterized by nuclear depletion and cytoplasmic aggregation of TAR DNA-binding protein-43 (TDP-43). TDP-43 plays a key role in regulating the splicing of numerous genes, including TARDBP. This review aims to delineate two aspects of ALS/FTD pathogenesis associated with TDP-43 function. First, we described novel mechanistic insights into...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aging
Share to Amyotrophic Lateral Sclerosis
Share to Amyotrophic Lateral Sclerosis Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA-Binding Proteins

Share to Frontotemporal Dementia

Share to Neurogenetic and Muscular Disorders Research

Share to Polymorphism, Single Nucleotide

Share to RNA Research and Splicing

Source

Identifiers

PMID: 38723906
DOI: 10.1016/j.neures.2024.05.001

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Molecular mechanisms linking loss of TDP-43 function to amyotrophic lateral sclerosis/frontotemporal dementia-related genes.PMID 38723906Read ↗

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A.Semantic proximity Read ↗

Decoding TDP-43: the molecular chameleon of neurodegenerative diseasesSemantic proximity Read ↗

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

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

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

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

TDP-43 represses cryptic exon inclusion in the FTD–ALS gene UNC13ASemantic proximity Read ↗

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

Understanding age-related pathologic changes in TDP-43 functions and the consequence on RNA splicing and signalling in health and diseaseSemantic proximity Read ↗

Connecting TDP-43 Pathology with Neuropathy.Semantic proximity Read ↗

Pathogenic TARDBP mutations in amyotrophic lateral sclerosis and frontotemporal dementia: disease-associated pathways.Semantic proximity Read ↗

The era of cryptic exons: implications for ALS-FTDSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.