Drug Screening for ALS Using Patient-Specific Induced Pluripotent Stem Cells

Naohiro Egawa(Kyoto University), Shiho Kitaoka(Kyoto University), Kayoko Tsukita(Kyoto University), Motoko Naitoh(Kyoto University), Kazutoshi Takahashi(Kyoto University), Takuya Yamamoto(Kyoto University), Fumihiko Adachi(Kyoto University), Takayuki Kondo(Kyoto University), Keisuke Okita(Kyoto University), Isao Asaka(Kyoto University), Takashi Aoi(Kyoto University), Akira Watanabe(Kyoto University), Yasuhiro Yamada(Kyoto University), Asuka Morizane(Kyoto University), Jun Takahashi(Kyoto University), Takashi Ayaki(Kyoto University), Hidefumi Ito(Kyoto University), Katsuhiro Yoshikawa(Kyoto University), Satoko Yamawaki(Kyoto University), Shigehiko Suzuki(Kyoto University), Dai Watanabe(Kyoto University), Hiroyuki Hioki(Kyoto University), Takeshi Kaneko(Kyoto University), Kouki Makioka(Gunma University), Koichi Okamoto(Gunma University), Hiroshi Takuma(University of Tsukuba), Akira Tamaoka(University of Tsukuba), Kazuko Hasegawa(National Sagamihara Hospital), Takashi Nonaka(Tokyo Metropolitan Institute of Medical Science), Masato Hasegawa(Tokyo Metropolitan Institute of Medical Science), Akihiro Kawata(Tokyo Metropolitan Neurological Hospital), Minoru Yoshida(RIKEN), Tatsutoshi Nakahata(Kyoto University), Ryōsuke Takahashi(Kyoto University), Maria C. Marchetto(Salk Institute for Biological Studies), Fred H. Gage(Salk Institute for Biological Studies), Shinya Yamanaka(Kyoto University), Haruhisa Inoue(Kyoto University)
Science Translational Medicine
August 1, 2012
Cited by 562

Abstract

Amyotrophic lateral sclerosis (ALS) is a late-onset, fatal disorder in which the motor neurons degenerate. The discovery of new drugs for treating ALS has been hampered by a lack of access to motor neurons from ALS patients and appropriate disease models. We generate motor neurons from induced pluripotent stem cells (iPSCs) from familial ALS patients, who carry mutations in Tar DNA binding protein-43 (TDP-43). ALS patient-specific iPSC-derived motor neurons formed cytosolic aggregates similar to those seen in postmortem tissue from ALS patients and exhibited shorter neurites as seen in a zebrafish model of ALS. The ALS motor neurons were characterized by increased mutant TDP-43 protein in a detergent-insoluble form bound to a spliceosomal factor SNRPB2. Expression array analyses detected small increases in the expression of genes involved in RNA metabolism and decreases in the expression of genes encoding cytoskeletal proteins. We examined four chemical compounds and found that a histone acetyltransferase inhibitor called anacardic acid rescued the abnormal ALS motor neuron phenotype. These findings suggest that motor neurons generated from ALS patient-derived iPSCs may provide a useful tool for elucidating ALS disease pathogenesis and for screening drug candidates.


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