miR-342-5p Decreases Ankyrin G Levels in Alzheimer’s Disease Transgenic Mouse Models

• miR-342-5p is upregulated in APP/PS1, PS1ΔE9, and PS1-M146V transgenic AD mice
• miR-342-5p upregulation is associated with elevated β-catenin, c-Myc, and IRF-9
• The increased miR-342-5p downregulates the expression of ankyrin G
• A specific microRNA alteration may contribute to AD axonopathy

SummaryMicroRNA alterations and axonopathy have been reported in patients with Alzheimer’s disease (AD) and in AD mouse models. We now report that miR-342-5p is upregulated in APP/PS1, PS1ΔE9, and PS1-M146V transgenic AD mice, and that this upregulation is mechanistically linked to elevated β-catenin, c-Myc, and interferon regulatory factor-9. The increased miR-342-5p downregulates the expression of ankyrin G (AnkG), a protein that is known to play a critical role at the axon initial segment. Thus, a specific miRNA alteration may contribute to AD axonopathy by downregulating AnkG.

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