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• W2017641504 abstract "In Japan, more than 700 000 people are suffering from schizophrenia and the total cost of schizophrenia in 2008 was calculated to be JPY 2.77 trillion.1 Although depression and dementia have recently gained attention in clinical psychiatry in Japan due to the marked increases in the numbers of patients with these conditions, innovation in the diagnosis and treatment of schizophrenia is also needed. Magnetic resonance imaging studies of schizophrenia patients have revealed gray matter reductions, predominantly in brain regions that roughly correspond to the components of the ‘social brain’, which subserves social cognitive processes. In this issue, a review of a series of structural neuroimaging studies by Fujiwara et al. (259–267) demonstrates that structural changes in the components that constitute the social brain are associated with several aspects of the social cognitive impairment seen in schizophrenia. Social cognition could be an important treatment target in schizophrenia because it is suggested to be more strongly and/or more directly linked with functional outcomes than clinical symptoms and neurocognition. Kusumi et al. (243–258) suggested that facilitating cortical neuroprotection and hippocampal neurogenesis could be potential mechanisms of action of atypical antipsychotic drugs (APD). If this is true, what are the clinical implications? Atypical APD are known to be more effective for negative symptoms and cognitive dysfunction than typical APD. If these important, but modest, clinical effects are mediated by the facilitation of neuroprotection and neurogenesis, it would be worthwhile examining whether neuroprotective and/or neurotrophic agents can restore the structural brain changes that may underlie the clinical symptoms and cognitive deficits in schizophrenia. Although the underlying mechanisms responsible for the structural brain alterations in schizophrenia remain to be elucidated, previous post-mortem brain studies and animal model studies have suggested that cortical apoptosis and increased oxidative stress might be involved in the pathophysiology of the condition. It has also been suggested that similarities exist between schizophrenia and neurodegenerative disorders, as was shown by Kota et al. (292–297), who reported shortened telomeres in the peripheral blood leukocytes of patients with unremitted schizophrenia. In recent years, much attention has been paid to the at-risk mental state for developing psychosis as a potential target for early intervention and prevention. As was reviewed by Karanikas et al. (268–282), the prolonged overproduction of cortisol and the resultant shift of hypothalamo–pituitary–adrenal axis activity might be one of the possible mechanisms for unmasking the underlying vulnerability to psychosis and also for accentuating brain damage in patients who are at risk of developing psychosis. If neuroprotective and/or neurotrophic strategies are found to be useful for treating schizophrenia, they should primarily target the earlier stages of the illness, including the prodromal phase, during which cognitive decline and progressive gray matter loss have been reported to occur. Antipsychotic medication, however, even atypical APD, are not primarily recommended for treating at-risk patients because of the unspecific nature of their diagnoses, which is reflected by the low transition rate to psychosis (32% in 3 years in a meta-analysis2), and the potential adverse effects of APD. Omega-3 polyunsaturated fatty acids have been reported to be promising candidates as potentially neuroprotective agents for the treatment to reduce the risk of progression to psychosis.3 Although DSM-5 finally excluded the ‘Attenuated Psychosis Syndrome’ from its official criteria, further research targeting the earlier clinical stages of schizophrenia is warranted. As is also seen in other Regular Articles and Letters in this issue, research of treatment, diagnosis, and pathogenesis of schizophrenia is making progress. We hope that innovation in psychiatric practice will ameliorate suffering from schizophrenia in forthcoming decades." @default.
• W2017641504 created "2016-06-24" @default.
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• W2017641504 date "2015-04-24" @default.
• W2017641504 modified "2023-09-27" @default.
• W2017641504 title "Targets in schizophrenia" @default.
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• W2017641504 doi "https://doi.org/10.1111/pcn.12292" @default.
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