Expression of amyloid-β in mouse cochlear hair cells causes an early-onset auditory defect in high-frequency sound perception

Yasuhiro Omata; Suganya Tharasegaran; Young-Mi Lim; Yasutoyo Yamasaki; Yasuhito Ishigaki; Takanori Tatsuno; Mitsuo Maruyama; Leo Tsuda

doi:doi:10.18632/aging.100899

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Research Paper Volume 8, Issue 3 pp 427—439

Expression of amyloid-β in mouse cochlear hair cells causes an early-onset auditory defect in high-frequency sound perception

Figure 1. Establishment of Tg mice expressing Aβ in cochlear hair cells. (A) Representative vector construction for the Tg mice used in this study. Tg(Math1^E-Aβ42)1Lt contains Aβ42 fused to the rat prepro-enkephalin secretion signal (sec) under the control of the Math1 minimal enhancer (Math1^E) and cytomegalovirus promoter. Tg(Math1^E-Aβ42^Arc)1Lt contains almost the same sequence as Tg(Math1^E-Aβ42)1Lt except that the sec-Aβ42^Arc sequence replaces sec-Aβ42. (B) Levels of Tg(Math1^E-Aβ42)1Lt and Tg(Math1^E-Aβ42^Arc)1Lt mRNAs from cochleae were measured by qPCR and normalized to the control (b-actin) in non-Tg mice. (C) ELISA of cochleae extracts from Tg(Math1^E-Aβ42^Arc)1Lt and non-Tg mice at age 4 months. S; Tris-buffered saline–soluble form, IS; insoluble (formic acid–soluble) form.