Cited by 106MicroRNA in disease regulationNeuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatments

Up-regulated Pro-inflammatory MicroRNAs (miRNAs) in Alzheimer’s disease (AD) and Age-Related Macular Degeneration (AMD)

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Pogue, Aileen I., Lukiw, Walter J.·2018·Cellular and Molecular Neurobiology

Abstract

Alzheimer's disease (AD) of the brain neocortex and age-related macular degeneration (AMD) of the retina are two complex neurodegenerative disorders, which (i) involve the progressive dysregulation and deterioration of multiple neurobiological signaling pathways, (ii) exhibit the temporal accumulation of pro-inflammatory lesions including the amyloid beta (Aβ) peptide-containing senile plaques of AD and the drusen of AMD, and (iii) culminate in an insidious inflammatory neurodegeneration ending, respectively, in neural cell atrophy and death and progressive loss of cognition and central visual function. Recent independent research studies have indicated that AD and AMD share common, pathological signaling defects and disease mechanisms at the molecular genetic level. Using high-integrity total RNA samples pooled from AD brain and AMD retina, microfluidic hybridization miRNA arrays, and bioinformatics, the current study was undertaken to quantify microRNA (miRNA) speciation and complexity common to both AD and AMD. These small non-coding (sncRNAs) are known to post-transcriptionally regulate multiple neurobiological pathways and an abundance of research information has already been generated on the roles of these miRNAs in pathological situations involving inflammatory neuropathology and neural cell decline. Here, for the first time, we report the sequence and abundance of a septet of sncRNAs including miRNA-7, miRNA-9-1, miRNA-23a/miRNA-27a, miRNA-34a, miRNA-125b-1, miRNA-146a, and miRNA-155 that are significantly increased in abundance and common to both AD-affected superior temporal lobe neocortex (Brodmann A22) and the AMD-affected macular region of the retina. Bioinformatics, miRNA-mRNA complementarity, next-gen RNA sequencing, and feature alignment analysis further indicate that these 7 up-regulated miRNAs have the potential to interact with and down-regulate ~ 9460 target messenger RNAs (mRNAs; about 3.5% of the genome) involved in the synchronization of amyloid production and clearance, phagocytosis, innate-immune, pro-inflammatory, and neurotrophic signaling and/or synaptogenesis in diseased tissues.

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Crossref · 10.1007/s10571-017-0572-3

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Authors
Pogue, A. I., & Lukiw, W. J.
Affiliations
Louisiana State University (US)
Corresponding author
Lukiw, Walter J.
Venue
Cellular and Molecular Neurobiology
Published
2018-01-04
Volume
38
Issue
5
Pages
1021-1031
ISSN
  • 0272-4340 (ISSN-L)
  • 1573-6830
OpenAlex
W2782487815
Cited by
105
References
72
Citations by year
2026: 4 · 2025: 5 · 2024: 13 · 2023: 10 · 2022: 17 · 2021: 18 · 2020: 14 · 2019: 14 · 2018: 10
FWCI
4.22
Type
journal article
Language
en
Open access
Locations
  • Cellular and Molecular Neurobiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute on Aging (AG18031, AG038834)
  • National Eye Institute (EY006311)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
Alzheimer's disease, age-related macular degeneration, microRNA, neuroinflammation, miRNA-mRNA interactions, amyloid-beta, drusen, retina, miR-34a, miRNA-146a, miR-155, innate immunity, synaptogenesis, neurodegeneration
MeSH terms
Alzheimer Disease, Base Sequence, Humans, Inflammation, Macular Degeneration, Up-Regulation, Oligonucleotide Array Sequence Analysis, MicroRNAs

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