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Cited by 160RNA regulation and diseaseAlzheimer's disease research and treatmentsRNA Research and Splicing

Reduced levels of protein recoding by A-to-I RNA editing in Alzheimer's disease

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Khermesh, Khen, D'Erchia, Anna Maria, Barak, Michal, Annese, Anita, Wachtel, Chaim, Levanon, Erez Y., Picardi, Ernesto, Eisenberg, Eli·2016·RNA
DOI 10.1261/rna.054627.115PMC PMC4712678
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Abstract

Adenosine to inosine (A-to-I) RNA editing, catalyzed by the ADAR enzyme family, acts on dsRNA structures within pre-mRNA molecules. Editing of the coding part of the mRNA may lead to recoding, amino acid substitution in the resulting protein, possibly modifying its biochemical and biophysical properties. Altered RNA editing patterns have been observed in various neurological pathologies. Here, we present a comprehensive study of recoding by RNA editing in Alzheimer's disease (AD), the most common cause of irreversible dementia. We have used a targeted resequencing approach supplemented by a microfluidic-based high-throughput PCR coupled with next-generation sequencing to accurately quantify A-to-I RNA editing levels in a preselected set of target sites, mostly located within the coding sequence of synaptic genes. Overall, editing levels decreased in AD patients’ brain tissues, mainly in the hippocampus and to a lesser degree in the temporal and frontal lobes. Differential RNA editing levels were observed in 35 target sites within 22 genes. These results may shed light on a possible association between the neurodegenerative processes typical for AD and deficient RNA editing.

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  • Four of these genes were involved in AD-related pathways such as Ca2+ permeability [GRIA2 and GRIK2], cellular dysfunction, and protein stability [NOVA1 and GIPC1].

    “Four of these genes were involved in AD-related pathways such as Ca2+ permeability [GRIA2 (55) and GRIK2 (29)], cellular dysfunction, and protein stability [NOVA1 (56) and GIPC1 (57)].”

    From Comprehensive characterization of the transcriptional landscape in Alzheimer’s disease (AD) brains (2025) · cites this paper as [29]

    The Discussion reports reduced GRIA2 RNA editing in Alzheimer’s disease, supporting GRIA2’s relevance to AD. The passages found do not link GRIA2 to Ca2+ permeability. In the printed sentence, the other genes have separate citations and are not attributed to this source. (LLM, conf=0.83)

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  • In BM36, altered A-to-I editing sites include GRIA2 (R/G and Q/R), GRIK2 (Q/R), and NOVA1 (S/G).

    “For example, in BM36, we identified well characterized A-to-I editing sites of GRIA2 (R/G and Q/R) (55, 75, 76) and GRIK2 (Q/R) (29, 77), as well as previously reported editing sites in NOVA1 (S/G) (29, 56) (Fig. 5D).”

    From Comprehensive characterization of the transcriptional landscape in Alzheimer’s disease (AD) brains (2025) · cites this paper as [29]

    The Discussion (page unavailable) reports reduced editing of GRIA2 in the temporal and frontal lobes of Alzheimer’s disease samples. It does not identify BM36 or substantiate the specified GRIA2 R/G and Q/R, GRIK2 Q/R, and NOVA1 S/G sites in BM36. Searches for BM36, GRIK2, and NOVA1 found no matching results in our copy. (LLM, conf=0.78)

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Authors
Khermesh, K., D'Erchia, A. M., Barak, M., Annese, A., Wachtel, C., Levanon, E. Y., Picardi, E., & Eisenberg, E.
Affiliations
  • Bar-Ilan University (IL)
  • University of Bari Aldo Moro (IT)
  • Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies (IT)
  • Tel Aviv University (IL)
ORCID
Venue
RNA
Publisher
Cold Spring Harbor Laboratory
Published
2015-12-11
Volume
22
Issue
2
Pages
290-302
ISSN
  • 1355-8382 (ISSN-L)
  • 1469-9001
DOI
10.1261/rna.054627.115
PMC
PMC4712678
OpenAlex
W2192293591
Cited by
160
References
86
Citations by year
2026: 9 · 2025: 14 · 2024: 17 · 2023: 22 · 2022: 15 · 2021: 21 · 2020: 19 · 2019: 10 · 2018: 20 · 2017: 9 · 2016: 3
FWCI
4.63
Type
journal article
Language
en
Open access
Locations
  • RNA (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
  • CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion, cc-by)
Funders
  • Ministry of Science, Technology and Space
  • Ministry of Foreign Affairs
  • European Research Council (311257)
  • I-CORE Program of the Planning and Budgeting Committee
  • Israel Science Foundation (41/11, 1796/12, 1380/14, 379/12)
  • Ministry of Science and Technology
  • Japan Science and Technology Agency (10765-3)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA regulation and disease
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
Keywords
A-to-I RNA editing, ADAR enzymes, Alzheimer's disease, synaptic genes, hippocampus, brain tissue, amino acid substitutions, neurodegeneration
MeSH terms
Adenosine, Adenosine Deaminase, Alzheimer Disease, Frontal Lobe, Hippocampus, Humans, Inosine, RNA Precursors, RNA, Double-Stranded, Temporal Lobe, Polymerase Chain Reaction, RNA-Binding Proteins, RNA Editing, Microfluidics, Epigenesis, Genetic, High-Throughput Nucleotide Sequencing

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