Cited by 44Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

RIG-1 receptor expression in the pathology of Alzheimer’s disease

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de Rivero Vaccari, Juan Pablo, Brand, Frank J, Sedaghat, Christina, Mash, Deborah C, Dietrich, W Dalton, Keane, Robert W·2014·Journal of Neuroinflammation

Abstract

BACKGROUND: Neuroinflammation plays a critical role in the pathogenesis of Alzheimer's disease (AD) and involves activation of the innate immune response via recognition of diverse stimuli by pattern recognition receptors (PRRs). The inflammatory inducers and precise innate signaling pathway contributing to AD pathology remain largely undefined. RESULTS: In the present study we analyzed expression levels of innate immune proteins in temporal and occipital cortices from preclinical (no cognitive impairment, NCI, N = 22) to mild cognitive impairment (MCI, N = 20) associated with AD pathology (N = 20) and AD patients (N = 23). We found that retinoic acid-inducible gene-I (RIG-1) is significantly elevated in the temporal cortex and plasma in patients with MCI. In addition, primary human astrocytes stimulated with the RIG-1 ligand 5'ppp RNA showed increased expression of amyloid precursor protein (APP) and amyloid-β (Aβ), supporting the idea that RIG-1 is involved in the pathology of MCI associated with early progression to AD. CONCLUSION: These findings suggest that RIG-1 may play a critical role in incipient AD.

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  • Previous reports show elevated RIG-I in the brains of patients with mild cognitive impairment.

    “Astrocytic dsRNA deposition is conserved in brains of tau transgenic mice and in patients with AD or PSP and occurs alongside elevation of the RIG-I-like dsRNA sensor MDA5 (Ochoa et al. 2023), consistent with previous reports of elevated RIG-I in the brains of patients with mild cognitive impairment (de Rivero Vaccari et al. 2014).”

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Authors
de Rivero Vaccari, J. P., Brand, F. J., Sedaghat, C., Mash, D. C., Dietrich, W. D., & Keane, R. W.
Affiliations
University of Miami (US)
Venue
Journal of Neuroinflammation
Published
2014-04-02
Volume
11
Issue
1
Pages
67-67
ISSN
1742-2094 (ISSN-L)
OpenAlex
W2151059472
Cited by
43
References
46
Citations by year
2026: 5 · 2025: 5 · 2024: 9 · 2022: 5 · 2021: 4 · 2020: 2 · 2018: 2 · 2017: 5 · 2016: 2 · 2015: 2 · 2014: 2
FWCI
2.44
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • University of Miami
  • University of Kentucky
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (R01NS042133, NS059836, R01NS059836, NS042133)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
RIG-I, Alzheimer's disease, mild cognitive impairment, neuroinflammation, innate immunity, pattern recognition receptors, amyloid-beta, amyloid precursor protein, astrocytes, temporal cortex, occipital cortex, plasma biomarkers
MeSH terms
DEAD Box Protein 58, Aged, Aged, 80 and over, Alzheimer Disease, Astrocytes, Cells, Cultured, Dose-Response Relationship, Drug, Female, Humans, Male, Middle Aged, Occipital Lobe, Peptide Fragments, Receptors, Immunologic, RNA, Viral, Temporal Lobe, Gene Expression, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Interferon Regulatory Factor-3, DEAD-box RNA Helicases, Cognitive Dysfunction

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