1989 Fiscal Year Final Research Report Summary
The Similarities and Differences of Biological Markers in Bipolar Disorders and Paranoid Schizophrenia
| Project/Area Number |
62480242
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Psychiatric science
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
WATANABE Akiko Tokyo Medical and Dental University,, 医学部・文部技官(教務職員) (40210992)
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| Co-Investigator(Kenkyū-buntansha) |
NANKAI Masahiro Tokyo Medical and Dental University, Teaching Staff., 医学部, 助手 (20218069)
KANENO Shigeru Tokyo Medical and Dental University, Teaching Staff., 医学部, 助手 (90126219)
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| Project Period (FY) |
1987 – 1989
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| Keywords | AFFECTIVE DISORDER / PARANOID SCHIZOPHRENIA / BETA-PHENYLETHYLAMINE / IMIPRAMINE BINDING / PAROXETINE BINDING / MONOAMINE OXIDASE / ヒト血小板 / ストレス |
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| Research Abstract |
Urinary beta-phenylethylamine ( PEA ), one of biological markers in both affective disorder and paranoid schizophrenia, was examined in rapid cycler bipolar disorder. Increase in urinary PEA was found preceding the switch from mania to depression. This finding suggests that PEA plays the role of a biological trigger in the switch mechanism of a rapid cycler, especially in the switch from mania to depression. Secondary, we studied the role of PEA in schizophrenia. Schizophrenia was divided into two types : paranoid and non-paranoid. Increased urinary PEA excretion was found only in paranoid schizophrenia. A relationship between platelet monoamine oxidase (MAO) activity and urinary PEA excretion was found. These results suggest that PEA plays different roles in bipolar disorder and schizophrenia.
We previously reported the mean maximum number of binding sites (Bmax) of imipramine in depressed patients was significantly lower than that in healthy controls. A significant negative correlation was found between the Bmax values and total scores of the 17-item Hamilton depression rating scale in major depression, but not in bipolar disorder. In this study, we investigated platelet paroxetine binding in bipolar disorder. But, the Bmax of paroxetine binding was not significantly decreased compared to that of healthy controls. The hypothesis that endogenous inhibitors acting on imipramine binding sites was discussed. Then, we studied controls and depressed patients to conform whether the activity of endogenous inhibitors acting on imipramine binding. But inhibition activities of the imipramine and paroxetine by serum from controls and depressed patients were similar.
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[Publications] Yoshimoto, S., Kaku, H., Shimogawa, S., Watanabe, A., Nakagawara, M. and Takahashi, R.: "Urinary Trace Amine Extraction and Platelet Monoamine Oxidase Activity in Schizophrenia." Psychiatry Research, Vol.21 229 - 236, 1987.
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[Publications] Yamada, S., Nankai, M., Yoshimoto, S., and Takahashi, R.: "The relationship between 14C-5HT uptake and 3H-paroxetine binding in the human platelets." The Japan Journal of Psychiatry and Neurology, Vol.42, 675, 1988.
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[Publications] Semba, J., Nankai, M., Maruyama, Y., Kaneno, S., Watanabe, A., and Takahashi, R.: "Increase in Urinary beta-Phenylethylamine Preceding the Switch from Mania to Depression : A "Rapid Cycler"." Clinical Psychiatry, Vol.176, 116 - 119, 1988.
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