- Multilateral research approach to mental health (clinical symptoms, genetic tests, blood tests, imaging, iPS cells, etc.)
- Discovery of disease biomarkers through basic and clinical research
- High-level clinical research and establishment of clinical guidelines
- Clinical database for dementia, schizophrenia and healthy subjects
- Molecular mechanisms for the onset of Alzheimer’s disease and frontaltemporal dementia
The adoptation of high-level clinical research and the construction of a clinical database for a multifaceted biological approach to mental health
Our laboratory specializes in the study of dementia, schizophrenia, sleep disorders, and developmental disorders. The research has led to the construction of a comprehensive clinical database that describes these diseases and disorders. The database has accumulated information from neuropsychological testing, imaging studies, tests on blood, cerebrospinal fluid, and the genome, etc. One example of the database is the SIPHONI-2 trial, which provided evidence for the benefits of lumboperitoneal shunt surgery for idiopathic normal pressure hydrocephalus pressure , leading to a revision of international guidelines. For mental disorders such as schizophrenia, we have built COCORO, which is a database of diverse phenotypes. Additionally, we demonstrated a schizophrenia-specific leftward asymmetry for pallidum volume . Also, treating schizophrenia with clozapine risks agranulocytosis. We could associate the risk of this potentially lethal side effect to patient HLA (human leukocyte antigen) using GWAS (genome-wide association analysis) .
Our work also aims to provide next generation infrastructure for the study of psychiatric disorders. For example, we are using ICT (information communication technology) and developing a good practice automatic extraction system for the collection of information to improve dementia care. Our work has even been featured on the prime minister’s official website.
Despite the number of patients with dementia and schizophrenia, very little is known about the onset mechanism. Regarding Alzheimer’s disease (AD), we are giving attention to the role of Aβ (amyloid β protein) and ways to prevent its plaque formation [4, 5]. This research includes the development of novel biomarkers for the disease. We have also discovered KLC1 splice variant E as an Aβ accumulation modifier by omics studies using mice and human studies. . Finally, regarding frontotemporal dementia, we have investigated the pathogenesis gene C9orf72 and revealed its translation into dipeptide-repeat protainits [7,8].
To learn more about our work, please see our website: http://www2.med.osaka-u.ac.jp/psy/laboratories/ for detailed research content and the latest information.
1. Kazui et al. Lancet Neurol. 14 (6): 585-594, 2015.
2. Okada et al. Molecular Psychiatry 21, 1460-1466, 2016.
3. Saito et al. Biological Psychiatry 80 (8): 636-42, 2016.
4. Okochi et al. EMBO J 21 (20): 5408-16, 2002.
5. Okochi et al. Cell Rep 3: 42-51, 2013.
6. Morihara et al. PNAS 111 (7): 2638-43, 2014.
7. Mori et al. Science 339 (6125): 1335-8, 2013.
8. Mori et al. EMBO Reports 17 (9): 1314-25, 2016.