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Impaired Neurogenesis as a Risk Factor for Schizophrenia and Related Mental Diseases

  • Chapter
Neurogenesis in the Adult Brain II

Abstract

Neurogenesis is a biological process with multiple steps, and it is critical in brain development and maintenance. The initial step in neurogenesis is the division of neural stem cells to renew themselves, simultaneously producing neuronally committed cells. The integrity of neurogenesis is vulnerable to both genetic and environmental factors. Etiological data imply that impairment in neurogenesis, which is possibly caused by genetic factors as well as by infection, stress, and low nutrition, may underlie the onset of mental diseases. In support of this, an intriguing association of abnormal hippocampal neurogenesis and deficits in prepulse inhibition (PPI), one of the compelling endophenotypes (biological markers) of mental disorders including schizophrenia, has been reported in various animal models. If impaired neurogenesis is truly a susceptibility factor for mental diseases, the restoration and improvement of neurogenesis may be beneficial. Here, we introduce an approach using fatty acids to restore neurogenesis. In the future, we hope that noninvasive imaging of neurogenesis will provide biological evidence for diagnosis, treatment, and prognosis of mental diseases.

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Acknowledgments

We thank Drs. Tatsunori Seki, Takeshi Sakurai, and Takeo Yoshikawa for critical comments on the manuscript. The work on which this review article is based was supported by a Grant-in-Aid for Scientific Research on Priority Areas, “Elucidation of Mechanisms Underlying Brain Development and Learning,” from the Core Research for Evolutional Science and Technology (CREST) of the Japanese Science and Technology Corporation (to N.O.). N.G. is supported by Tohoku Neuroscience Global COE.

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Osumi, N., Guo, N. (2011). Impaired Neurogenesis as a Risk Factor for Schizophrenia and Related Mental Diseases. In: Seki, T., Sawamoto, K., Parent, J.M., Alvarez-Buylla, A. (eds) Neurogenesis in the Adult Brain II. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53945-2_6

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