ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2021
Long genes are more frequently affected by somatic mutations and show reduced expression in Alzheimer's disease: Implications for disease etiology.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Mega-enhancers compartmentalize transcriptionally active long genes in the brain.Nature cell biology · 2026Article
- When R-Loops Go Awry: Genome Instability and Neurological Diseases.The European journal of neuroscience · 2026Review
- Brain somatic mutations in Alzheimer's disease: linking genetic mosaicism to neurodegeneration.Molecular neurodegeneration · 2025Review
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- DeepDrug as an expert guided and AI driven drug repurposing methodology for selecting the lead combination of drugs for Alzheimer's disease.Scientific reports · 2025Article
- Transcriptional stress in aging: integrating experimental data and modeling to quantify DNA damage accumulation.Frontiers in molecular biosciences · 2025Article
- Improved health by combining dietary restriction and promoting muscle growth in DNA repair-deficient progeroid mice.Journal of cachexia, sarcopenia and muscle · 2024Article
- Inflammation and DNA methylation in Alzheimer's disease: mechanisms of epigenetic remodelling by immune cell oxidants in the ageing brain.Redox report : communications in free radical research · 2024Review
- Molecular landscape of the overlap between Alzheimer's disease and somatic insulin-related diseases.Alzheimer's research & therapy · 2024Article
- Frontotemporal lobar degeneration targets brain regions linked to expression of recently evolved genes.Brain : a journal of neurology · 2024Article
- DNA Damage and Parkinson's Disease.International journal of molecular sciences · 2024Review
- Time is ticking faster for long genes in aging.Trends in genetics : TIG · 2024Review
- Transcriptomics : Approaches to Quantifying Gene Expression and Their Application to Studying the Human Brain.Current topics in behavioral neurosciences · 2024Review
- A review and analysis of key biomarkers in Alzheimer's disease.Frontiers in neuroscience · 2024Review
- FTLD targets brain regions expressing recently evolved genes.medRxiv : the preprint server for health sciences · 2023Article
- Sting and p53 DNA repair pathways are compromised in Alzheimer's disease.Scientific reports · 2023Article
- Age or lifestyle-induced accumulation of genotoxicity is associated with a length-dependent decrease in gene expression.iScience · 2023Article
- The Road Less Traveled: Uncovering the Convergence Toward Specific Pleiotropic Phenotypes in Aging.bioRxiv : the preprint server for biology · 2023Article
- Genome-wide RNA polymerase stalling shapes the transcriptome during aging.Nature genetics · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Aging, the greatest risk factor for Alzheimer's disease (AD), may lead to the accumulation of somatic mutations in neurons. We investigated whether somatic mutations, specifically in longer genes, are implicated in AD etiology. First, we modeled the theoretical likelihood of genes being affected by aging-induced somatic mutations, dependent on their length. We then tested this model and found that long genes are indeed more affected by somatic mutations and that their expression is more frequently reduced in AD brains. Furthermore, using gene-set enrichment analysis, we investigated the potential consequences of such long gene disruption. We found that long genes are involved in synaptic adhesion and other synaptic pathways that are predicted to be inhibited in the brains of AD patients. Taken together, our findings indicate that long gene-dependent synaptic impairment may contribute to AD pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.