ArticleMolecular neurobiology2018
Overexpression of LINE-1 Retrotransposons in Autism Brain.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
55 citing papers in PubMed, 95 citations in OpenAlex.
- Early maternal care restores LINE-1 methylation and enhances neurodevelopment in preterm infants.BMC medicine · 2021Trial
- Review
- Plasma EV LINE-1 mRNA as a diagnostic biomarker for differentiating Alzheimer's disease from non-Alzheimer's dementias.Alzheimer's research & therapy · 2026Article
- Role of LINE-1 in the nervous system and neurological disorders.Chinese medical journal · 2026Review
- Radiofrequency regulates the BET-mediated pathways in radial glia differentiation in human cortical development.Cell reports · 2025Article
- Transposable elements as instructors of the immune system.Nature reviews. Immunology · 2025Review
- Sequence Diversity and Encoded Enzymatic Differences of Monocistronic L1 ORF2 mRNA Variants in the Aged Normal and Alzheimer's Disease Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Retrotransposon: an insight into neurological disorders from perspectives of neurodevelopment and aging.Translational neurodegeneration · 2025Review
- Transposon activity and nucleotide triplet instability: new perspectives on their potential interplay in brain disorders.Frontiers in neuroscience · 2025Article
- Transcripts derived from AmnSINE1 repetitive sequences are depleted in the cortex of autism spectrum disorder patients.Frontiers in bioinformatics · 2025Article
- Widespread transposable element dysregulation in human aging brains with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Investigation of chimeric transcripts derived from LINE-1 and Alu retrotransposons in cerebellar tissues of individuals with autism spectrum disorder (ASD).Scientific reports · 2024Article
- Retrotransposons in embryogenesis and neurodevelopment.Biochemical Society transactions · 2024Review
- Association of Relative Telomere Length and LINE-1 Methylation with Autism but not with Severity.Journal of autism and developmental disorders · 2024Article
- Condensin-mediated restriction of retrotransposable elements facilitates brain development in Drosophila melanogaster.Nature communications · 2024Article
- Detection of APP gene recombinant in human blood plasma.Scientific reports · 2023Article
- Review
- Exploratory analysis of L1 retrotransposons expression in autism.Molecular autism · 2023Article
- Epigenetic Gene-Regulatory Loci in Alu Elements Associated with Autism Susceptibility in the Prefrontal Cortex of ASD.International journal of molecular sciences · 2023Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Long interspersed nuclear elements-1 (LINE-1 or L1) are mobile DNA sequences that are capable of duplication and insertion (retrotransposition) within the genome. Recently, retrotransposition of L1 was shown to occur within human brain leading to somatic mosaicism in hippocampus and cerebellum. Because unregulated L1 activity can promote genomic instability and mutagenesis, multiple mechanisms including epigenetic chromatin condensation have evolved to effectively repress L1 expression. Nonetheless, L1 expression has been shown to be increased in patients with Rett syndrome and schizophrenia. Based on this evidence and our reports of oxidative stress and epigenetic dysregulation in autism cerebellum, we sought to determine whether L1 expression was increased in autism brain. The results indicated that L1 expression was significantly elevated in the autism cerebellum but not in BA9, BA22, or BA24. The binding of repressive MeCP2 and histone H3K9me3 to L1 sequences was significantly lower in autism cerebellum suggesting that relaxation of epigenetic repression may have contributed to increased expression. Further, the increase in L1 expression was inversely correlated with glutathione redox status consistent with reports indicating that L1 expression is increased under pro-oxidant conditions. Finally, the expression of transcription factor FOXO3, sensor of oxidative stress, was significantly increased and positively associated with L1 expression and negatively associated with glutathione redox status. While these novel results are an important first step, future understanding of the contribution of elevated L1 expression to neuronal CNVs and genomic instability in autism will depend on emerging cell-specific genomic technologies, a challenge that warrants future investigation.
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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.