ReviewJournal of neurology, neurosurgery, and psychiatry2019
Retrotransposons in the development and progression of amyotrophic lateral sclerosis.
Review in Journal of neurology, neurosurgery, and psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Environmental risk factors, protective factors, and biomarkers for amyotrophic lateral sclerosis: an umbrella review.Frontiers in aging neuroscience · 2025Pooled it
- LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- Classification of ALS molecular subtypes: a literature review on machine learning applications and their clinical value.BMC medicine · 2026Review
- The Other Side of the Same Coin: Beyond the Coding Region in Amyotrophic Lateral Sclerosis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Deep Intronic SVA_E Insertion Identified as the Most Common Pathogenic Variant Associated With Canavan Disease: A Diagnostic Blind Spot.Neurology. Genetics · 2025Article
- Review
- Tandem repeat expansions and copy number variations as risk factors and diagnostic tools for amyotrophic lateral sclerosis.Frontiers in neurology · 2025Review
- Comprehensive identification of pathogenic tandem repeat expansions in sporadic amyotrophic lateral sclerosis: advantages of long-read vs. short-read sequencing.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Retrotransposition-competent L1s are increased in the genomes of individuals with amyotrophic lateral sclerosis.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Exploring SVA Insertion Polymorphisms in Shaping Differential Gene Expressions in the Central Nervous System.Biomolecules · 2024Article
- Transposable Elements: Emerging Therapeutic Targets in Neurodegenerative Diseases.Neurotoxicity research · 2024Review
- Transcriptomic profiling of cerebrospinal fluid identifies ALS pathway enrichment and RNA biomarkers in MND individuals.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Human Endogenous Retrovirus-K (HML-2)-Related Genetic Variation: Human Genome Diversity and Disease.Genes · 2023Review
- A Genome-Wide Screen for the Exonisation of Reference SINE-VNTR-Alus and Their Expression in CNS Tissues of Individuals with Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Article
- Pathways to healing: Plants with therapeutic potential for neurodegenerative diseases.IBRO neuroscience reports · 2023Article
- Human leukocyte antigen super-locus: nexus of genomic supergenes, SNPs, indels, transcripts, and haplotypes.Human genome variation · 2022Review
- Integration of TE Induces Cancer Specific Alternative Splicing Events.International journal of molecular sciences · 2022Review
- Locus specific reduction of L1 expression in the cortices of individuals with amyotrophic lateral sclerosis.Molecular brain · 2022Article
- Transcription start site signal profiling improves transposable element RNA expression analysis at locus-level.Frontiers in genetics · 2022Article
- Characterisation of the Function of a SINE-VNTR-Frontiers in molecular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Endogenous retrotransposon sequences constitute approximately 42% of the human genome, and mobilisation of retrotransposons has resulted in rearrangements, duplications, deletions, novel transcripts and the introduction of new regulatory domains throughout the human genome. Both germline and somatic de novo retrotransposition events have been involved in a range of human diseases, and there is emerging evidence for the modulation of retrotransposon activity during the development of specific diseases. Particularly, there is unequivocal consensus that endogenous retrotransposition can occur in neuronal lineages. This review addresses our current knowledge of the different mechanisms through which retrotransposons might influence the development of and predisposition to amyotrophic lateral sclerosis.
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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.