期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 16, 期 12, 页码 30105-30116出版社
MDPI
DOI: 10.3390/ijms161226223
关键词
A beta 2 peptide; age-related macular degeneration (AMD); amyloid clearance; heterogeneity of the disease process; inflammation; innate-immune response; microRNA (miRNA); miRNA-7; miRNA-9; miRNA-34a; miRNA-125b; miRNA-146a; miRNA-155; normal aging; prion disease; sporadic AD
资金
- NIH/NIA [P50 AG16573]
- Research to Prevent Blindness (RPB)
- Louisiana Biotechnology Research Network (LBRN)
- NIH [NEI EY006311, NIA AG18031, NIA AG038834]
Of the approximately similar to 2.65 x 10(3) mature microRNAs (miRNAs) so far identified in Homo sapiens, only a surprisingly small but select subsetabout 35-40are highly abundant in the human central nervous system (CNS). This fact alone underscores the extremely high selection pressure for the human CNS to utilize only specific ribonucleotide sequences contained within these single-stranded non-coding RNAs (ncRNAs) for productive miRNA-mRNA interactions and the down-regulation of gene expression. In this article we will: (i) consolidate some of our still evolving ideas concerning the role of miRNAs in the CNS in normal aging and in health, and in sporadic Alzheimer's disease (AD) and related forms of chronic neurodegeneration; and (ii) highlight certain aspects of the most current work in this research field, with particular emphasis on the findings from our lab of a small pathogenic family of six inducible, pro-inflammatory, NF-B-regulated miRNAs including miRNA-7, miRNA-9, miRNA-34a, miRNA-125b, miRNA-146a and miRNA-155. This group of six CNS-abundant miRNAs significantly up-regulated in sporadic AD are emerging as what appear to be key mechanistic contributors to the sporadic AD process and can explain much of the neuropathology of this common, age-related inflammatory neurodegeneration of the human CNS.
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