Abnormal splicing of multiple exons in microtubule associated protein tau (MAPT), and exon 7 in the amyloid precursor protein (APP) and exon 5 in glutamate receptor NMDAR1, have been detected in brains of DM1 patients and mouse models (Jiang et al., 2004; Gomes-Pereira et al., 2007) and analogous splicing alterations have been shown in SCA8 mice (Daughters et al., 2009) which may explain neurological alterations in these diseases. The gene discussed is APP; the disease is myotonic dystrophy type 1.