Idiopathic carbonyl stress in a subpopulation of schizophrenia

Presentation First Author: 
Makotoi Ara

Evidence based on biological treatment and psychosocial support is essential to achieve and maintain a recovery for patients with schizophrenia. Studies have attempted to clarify the underlying disease mechanisms, however, the main cause and pathophysiology of schizophrenia remains unclear. Especially, heterogeneity in schizophrenia makes the search for molecular mechanisms much more difficult due to biochemical differences, variability across clinical symptoms, courses of illness, presence of risk factors and treatment responses. Although an improvement of positive symptoms of schizophrenia is progressing by developing atypical antipsychotics, the launch of new drugs for unmet medical needs is expected to improve cognitive dysfunctions and recovery of negative symptoms for patients with schizophrenia. Accumulation of toxic reactive dicarbonyls such as methylglyoxal, which are referred to as carbonyl stress, result in the modification of proteins and the formation of advanced glycation end products such as pentosidine. On June 2010, we have reported idiopathic carbonyl stress in a subpopulation of schizophrenia, leading to a failure of metabolic systems with plasma pentosidine accumulation and serum pyridoxal depletion. Our findings suggest that two markers, pentosidine and pyridoxal, are beneficial for distinguishing a subgroup from patients of the disease. We believe that the beneficial information covering from in vitro to in vivo lead to more suitable personalized medicine for schizophrenia. In my talk, I would like to provide a brief overview of carbonyl stress-induced schizophrenia, and discuss heterogeneity of schizophrenia covering an in vivo and an in vitro study in progress.

Conference Name: 
Presentation Date: 
January, 2015
Additional Authors: 
Mitsuhiro Miyashita - Akiko Kobori - Kazuya Toriumi - Yasue Horiuchi - Naila Rabbani - Paul Thornalley - Masanari Itokawa
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