ReviewChromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology2018
Warning SINEs: Alu elements, evolution of the human brain, and the spectrum of neurological disease.
Review in Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Differential A-to-I editing of SINE B2 RNAs unveils an epitranscriptome response to Aβ neurotoxicity.Life science alliance · 2026Article
- Pre-analytical storage effects on ALU- and LINE1-derived cell-free DNA biomarkers in whole blood and plasma.Biomolecules & biomedicine · 2026Article
- Primate-specific adaptation of Ku protects transcriptomic integrity by suppressing Alu-mediated alternative splicing.bioRxiv : the preprint server for biology · 2025Article
- Epigenetic dysregulation of transposable elements in cognitive impairment and Alzheimer's disease.GeroScience · 2025Article
- Single-Cell Transcriptome Patterns of Transposable Elements in Alzheimer's Disease.Molecular neurobiology · 2025Article
- Transposable elements in health and disease: Molecular basis and clinical implications.Chinese medical journal · 2025Review
- Article
- Article
- Emerging Functions of the Repeat Genome in Nuclear Structure: A View from the Human Karyotype.Annual review of genomics and human genetics · 2025Review
- Review
- The Flipons, Infections, and Amyloids that Foreshadow the Fading Memories of Alzheimer's Disease.Neuroscience insights · 2025Review
- Transcripts derived from AmnSINE1 repetitive sequences are depleted in the cortex of autism spectrum disorder patients.Frontiers in bioinformatics · 2025Article
- The Human Developing Cerebral Cortex Is Characterized by an Elevated De Novo Expression of Long Noncoding RNAs in Excitatory Neurons.Molecular biology and evolution · 2024Article
- Retrotransposons in embryogenesis and neurodevelopment.Biochemical Society transactions · 2024Review
- Mitochondrial genome plasticity of mammalian species.BMC genomics · 2024Article
- Polyamine Dysregulation and Nucleolar Disruption in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Article
- Neurodegenerative diseases reflect the reciprocal roles played by retroelements in regulating memory and immunity.Frontiers in neuroscience · 2024Article
- Epigenetic Gene-Regulatory Loci in Alu Elements Associated with Autism Susceptibility in the Prefrontal Cortex of ASD.International journal of molecular sciences · 2023Article
- Article
- Exonized Alu repeats in the 3'UTR of a CYP20A1_Alu-LT transcript act as a miRNA sponge.BMC research notes · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alu elements are a highly successful family of primate-specific retrotransposons that have fundamentally shaped primate evolution, including the evolution of our own species. Alus play critical roles in the formation of neurological networks and the epigenetic regulation of biochemical processes throughout the central nervous system (CNS), and thus are hypothesized to have contributed to the origin of human cognition. Despite the benefits that Alus provide, deleterious Alu activity is associated with a number of neurological and neurodegenerative disorders. In particular, neurological networks are potentially vulnerable to the epigenetic dysregulation of Alu elements operating across the suite of nuclear-encoded mitochondrial genes that are critical for both mitochondrial and CNS function. Here, we highlight the beneficial neurological aspects of Alu elements as well as their potential to cause disease by disrupting key cellular processes across the CNS. We identify at least 37 neurological and neurodegenerative disorders wherein deleterious Alu activity has been implicated as a contributing factor for the manifestation of disease, and for many of these disorders, this activity is operating on genes that are essential for proper mitochondrial function. We conclude that the epigenetic dysregulation of Alu elements can ultimately disrupt mitochondrial homeostasis within the CNS. This mechanism is a plausible source for the incipient neuronal stress that is consistently observed across a spectrum of sporadic neurological and neurodegenerative disorders.
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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.