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The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.

Neurodegeneration, Heterochromatin, and Double-Stranded RNA

Saldi, Tassa K, Gonzales, Patrick K, LaRocca, Thomas J, Link, Christopher D·2019·Journal of Experimental Neuroscience
DOI 10.1177/1179069519830697PMC PMC6376497
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Abstract

Changes in chromatin and epigenetic modifications have been associated with aging and aging-associated neurodegenerative diseases, although the causal relationship between these changes and disease-related pathology has been unclear. Recent studies have now made direct connections between neurodegeneration-associated proteins and derepression of repetitive element transcription due to changes in heterochromatin. We suggest that this derepression leads to an increased accumulation of intracellular double-stranded RNA (dsRNA), with an attendant induction of innate immune responses that contribute to the neuroinflammation found in essentially all age-associated neurodegenerative diseases.

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Figures

Figure 1. Model for how depletion of TDP-43 leads to increased accumulation of dsRNA. Speculative model based on C elegans studies illustrating how the nuclear depletion of TDP-43 observed in neurons and glia in ALS/FTD patients could lead to accumulation of dsRNA and upregulation of innate immune responses. ALS indicates amyotrophic lateral sclerosis; dsRNA, double-stranded RNA; FTD, frontotemporal dementia; TDP-43, Tar DNA binding protein 43 kd.
Figure 1. Model for how depletion of TDP-43 leads to increased accumulation of dsRNA. Speculative model based on C elegans studies illustrating how the nuclear depletion of TDP-43 observed in neurons and glia in ALS/FTD patients could lead to accumulation of dsRNA and upregulation of innate immune responses. ALS indicates amyotrophic lateral sclerosis; dsRNA, double-stranded RNA; FTD, frontotemporal dementia; TDP-43, Tar DNA binding protein 43 kd.CC BY-NC · PubMed Central
Figure 2. Increased repetitive elements and RNA editing in AD frontal cortex. (A) MA plot of relative RE abundance based on reanalysis of published RNA-seq data (Scheckel et al16) from postmortem frontal cortex. MA plots are typically used to visualize gene expression changes by plotting the log of the expression ratios between experimental and control samples against mean average expression levels for each gene. Here we plot the log ratio of expression for individual repetitive element classes calculated from patient and control RNA-seq data. Note both the overall shift of the expression ratios to positive log values (ie, up in AD patients) and the set of RE with statistically-significant transcript abundance over-represented in AD brains (red circle). (B) Average number of adenosine-to-inosine edited reads in the same RNA-seq data. AD indicates Alzheimer disease; RNA-seq, global transcriptome analysis high-throughput sequencing. Error bar = SEM; *P < .05.
Figure 2. Increased repetitive elements and RNA editing in AD frontal cortex. (A) MA plot of relative RE abundance based on reanalysis of published RNA-seq data (Scheckel et al16) from postmortem frontal cortex. MA plots are typically used to visualize gene expression changes by plotting the log of the expression ratios between experimental and control samples against mean average expression levels for each gene. Here we plot the log ratio of expression for individual repetitive element classes calculated from patient and control RNA-seq data. Note both the overall shift of the expression ratios to positive log values (ie, up in AD patients) and the set of RE with statistically-significant transcript abundance over-represented in AD brains (red circle). (B) Average number of adenosine-to-inosine edited reads in the same RNA-seq data. AD indicates Alzheimer disease; RNA-seq, global transcriptome analysis high-throughput sequencing. Error bar = SEM; *P < .05.CC BY-NC · PubMed Central

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Research works printed but not linked: 6

  1. 10.1126/science.1134108 · DOI · Paper page
  2. 10.1128/MCB.00668-17 · DOI · Paper page
  3. 10.1101/gr.180489.114 · DOI
  4. 10.7554/eLife.21666 · DOI
  5. 10.1134/S0006297917080120 · DOI
  6. Rodriguez S, Schrank BR, Sahin A, et al. Genome-encoded cytoplasmic double-stranded RNAs, found in C9ORF72 ALS-FTD brain, provoke propagated neuronal death. BioRvix 248328 (Preprint). https://www.biorxiv.org/content/early/2018/01/19/248328. Published January 19, 2018. Accessed November 7, 2018. · DOI

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Metadata

Authors
Saldi, T. K., Gonzales, P. K., LaRocca, T. J., & Link, C. D.
Affiliations
  • Department of Biochemistry and Molecular Genetics, University of Colorado, Aurora, CO, USA
  • Department of Integrative Physiology, University of Colorado, Boulder, CO, USA
ORCID
Link, Christopher D
Venue
Journal of Experimental Neuroscience
Publisher
SAGE Publications
Published
2019-01
Volume
13
ISSN
1179-0695
DOI
10.1177/1179069519830697
PMC
PMC6376497
Cited by
20
References
12
Language
en
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Funders
National Institute of Neurological Disorders and Stroke (R01 AG061387)

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CoChat. (2026). Citation check: Neurodegeneration, Heterochromatin, and Double-Stranded RNA. https://app.cochat.ai/papers/10.1177/1179069519830697
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Saldi, T. K., Gonzales, P. K., LaRocca, T. J., & Link, C. D. (2019). Neurodegeneration, Heterochromatin, and Double-Stranded RNA. Journal of Experimental Neuroscience. https://doi.org/10.1177/1179069519830697

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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