Discover Community Create You

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

Non-coding genome contribution to ALS.

International review of neurobiology - 1 Jan 2024

Moll Tobias, Harvey Calum, Alhathli Elham, Gornall Sarah, O'Brien David, Cooper-Knock Johnathan

Abstract excerpt

The majority of amyotrophic lateral sclerosis (ALS) is caused by a complex gene-environment interaction. Despite high estimates of heritability, the genetic basis of disease in the majority of ALS patients are unknown. This limits the development of targeted genetic therapies which require an understanding of patient-specific genetic drivers. There is good evidence that the majority of these missing genetic risk...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis
Share to TBK1 gene
Share to Genetic Predisposition to Disease

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 38802183
DOI: 10.1016/bs.irn.2024.04.002

Genes

TBK1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Non-coding genome contribution to ALS.PMID 38802183Read ↗

Genome-wide Identification of the Genetic Basis of Amyotrophic Lateral SclerosisSemantic proximity Read ↗

Genome-wide identification of the genetic basis of amyotrophic lateral sclerosisSemantic proximity Read ↗

ALS Genes in the Genomic Era and their Implications for FTD.Semantic proximity Read ↗

Characterising the Genetic Landscape of Amyotrophic Lateral Sclerosis: A Catalogue and Assessment of Over 1,000 Published Genetic VariantsSemantic proximity Read ↗

Wild-type <i>C9orf72</i> expression is a genetic modifier of C9-ALS survivalSemantic proximity Read ↗

Genetic analysis of amyotrophic lateral sclerosis identifies contributing pathways and cell typesSemantic proximity Read ↗

Partitioning the genetic architecture of amyotrophic lateral sclerosisSemantic proximity Read ↗

Enrichment of rare protein truncating variants in amyotrophic lateral sclerosis patientsSemantic proximity Read ↗

Common and rare variant association analyses in Amyotrophic Lateral Sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biologySemantic proximity Read ↗

Rare variant burden analysis within enhancers identifies CAV1 as an ALS risk geneSemantic proximity Read ↗

The New York Genome Center ALS Consortium resource integrates postmortem tissue transcriptomics and whole genome sequencing to empower biological discoverySemantic proximity Read ↗

The non-specific lethal complex regulates genes and pathways genetically linked to Parkinson’s diseaseSemantic proximity Read ↗

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