Letters To The Editor
- Dlouhy et al. (1) recently refined how β-amyloid precursor protein (APP)2 participates in iron (Fe) efflux and hinted that APP may be unnecessary for ferroportin-supported Fe efflux. APP and Fe efflux have long been our interest, given recent work on the APP mRNA 5′-UTR and how regulation of APP translation operates through an interleukin-1 acute box, an iron response element (IRE), where iron-responsive protein 1 (IRP1) binds, and a target sequence for microRNA-346 (2). Untangling the roles of IRE, IRP1, interleukin-1, and miR-346 at the APP 5′-UTR is critical in Alzheimer’s disease (AD).
- As neuroscientists, we were intrigued when Huang et al. (1) reported that miR101 can attenuate pulmonary fibrosis (PF)2 through suppression of Wnt family member 5A (WNT5A). Accumulating evidence suggests that prima facie unrelated disorders in multiple fields of medicine share fundamental molecular pathways. For example, PF associates with cognitive impairment (2). It is reasonable to presume that such links would be due to hypoxia and general inflammation, but could there be a deeper connection? Both miR101 and miR27b expression levels were significantly reduced in more severe PF cases (1).