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Early onset of inflammation during ontogeny of bipolar disorder: the NLRP2 inflammasome gene distinctly differentiates between patients and healthy controls in the transition between iPS cell and neural stem cell stages

Journal article
Authors Dzeneta Vizlin-Hodzic
Qiwei Zhai
Sebastian Illes
Kristoffer Södersten
Katarina Truvé
Toshima Z Parris
Praveen Sobhan
Susanne Salmela
Subazini Kosalai
Chandrasekhar Kanduri
Joakim Strandberg
Henrik Seth
Thomas Bontell
Eric Hanse
Hans Ågren
Keiko Funa
Published in Translational Psychiatry
Volume 7
Publication year 2017
Published at Institute of Biomedicine, Department of Medical and Clinical Genetics
Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Physiology
Sahlgrenska Cancer Center
Institute of Biomedicine
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Core Facilities, Bioinformatics
Institute of Clinical Sciences, Department of Radiology
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Language en
Keywords NLPR2, inflammasome, bipolar disorder, iPS model, transcriptome
Subject categories Neuroscience, Cell and Molecular Biology, Medical Genetics


Neuro-inflammation and neuronal communication are considered as mis-regulated processes in the aetiology and pathology of bipolar disorder (BD). Which and when specific signal pathways become abnormal during the ontogeny of bipolar disorder patients is unknown. To address this question, we applied induced pluripotent stem cell (iPSC) technology followed by cortical neural differentiation on adipocyte-derived cells from BD type I patients (with psychotic episodes in psychiatric history) and healthy volunteers (controls). RNA sequencing in iPSC and cortical neural stem cell (NSC) lines were used to examine alterations between the transcriptomes from BD I and control samples during transition from the pluripotent stage towards the neural developmental stage. At the iPSC stage, the most highly significant differentially expressed gene (DEG) was the NLRP2 inflammasome (P = 2.66 × 10-10). Also among 42 DEGs at the NSC stage, NLRP2 showed the strongest statistical significance (P = 3.07 × 10-19). In addition, we have also identified several cytoskeleton-associated genes as DEGs from the NSC stage, such as TMP2, TAGLN, and ACTA2; the former two genes are recognised for the first time to be associated with BD. Our results also suggest that iPSC-derived BD-cortical NSCs carry several abnormalities in dopamine and GABA receptor canonical pathways, underlining that our in vitro BD model reflects pathology in the CNS. This would indicate that mis-regulated gene expression of inflammatory, neurotransmitter, and cytoskeletal signalling occurs during early foetal brain development of BD I patients.

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