A study of pathology and therapy of the dementia associated with testosterone supplementation-refractory late onset hypogonadism syndrome

Research Project

Project/Area Number	26860135
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	General anatomy (including histology/embryology)
Research Institution	University of Occupational and Environmental Health, Japan (2015) Yamaguchi University (2014)
Principal Investigator	KOKUBU Keiji 産業医科大学, 医学部, 助教 (00432740)
Project Period (FY)	2014-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000) Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000) Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords	男性更年期障害 / 芳香化酵素 / アンドロゲン / エストロゲン / エストロゲン受容体 / 扁桃体 / テストステロン / アロマテース / 性ステロイドホルモン
Outline of Final Research Achievements	Aromatase which create estrogen from testosterone and two types of estrogen receptor (ERα and ERβ) are expressed in the medial amygdaloid nucleus of the brain. Therefore, it is expected that the brains of men is influenced by estrogen than the women brain. In the medial amygdaloid nucleus of the castrated male rats used as a model of the male menopause, the quantity of ERα protein was increased in comparison with sham-operated rats. The administration of testosterone or estrogen to the castrated rat decreased ERα protein again. In contrast, the administration of the dihydrotestosterone which was a kind of androgen did not affect the quantity of ERα. The quantity of the ER β protein was stable without being affected by castration and any sex steroidal hormones.