Abstract
Transfer RNA-derived fragments (tRFs) are known to contribute to multiple illnesses, including cancers, viral infections, and age-related neurodegeneration. In this study, we used senescence-accelerated mouse prone 8 (SAMP8) as a model of neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, and a control, the senescence-accelerated mouse resistant 1 (SAMR1) model, to comprehensively explore differences in tRF expression between them. We discovered 570 tRF transcripts among which eight were differentially expressed. We then obtained 110 potential target genes in a miRNA-like pattern. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation suggest that these target genes participate in a variety of brain functions; e.g., synapse formation (GO: 0045202) and the synaptic vesicle cycle pathway. We further assessed in detail those tRFs whose miRNA-like pattern was most likely to promote the progression of either Alzheimer’s or Parkinson’s disease, such as AS-tDR-011775 acting on Mobp and Park2. Our findings suggest the eight dysregulated tRFs we uncovered here may be beneficially exploited as potential diagnostic biomarkers and/or therapeutic targets to treat age-related brain diseases.
Highlights
Changes occur in all parts of a person’s body, including the brain, during aging
senescence-accelerated mouse prone 8 (SAMP8) mice exhibit a decline of learning and memory at the 7-month stage
SAMP8 mice took a longer time to find the platform than senescence-accelerated mouse resistant 1 (SAMR1) mice (p < 0.05)
Summary
The brain naturally shrinks in volume, and an increased size of the brain sulci with age is observed [1] These changes have significant impacts on learning and other complex mental activities. Brain aging and neurodegeneration appear to go hand in hand, especially in Alzheimer’s disease (AD) and Parkinson’s disease (PD) [2] Some countries, such as China, Japan, and Italy, have become aging societies that have considered the problem of aiding the aging brain to prevent related diseases as a public concern. Many theories such as Aβ deposition and tau phosphorylation in AD [3] and alpha-synuclein aggregation in PD [4] have attempted to explain the causes of these pathologies. In spite of the knowledge gained concerning the etiology of AD and PD in the last several decades, few treatments are available to prevent them
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