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ACE activity in CSF of patients with MCI, AD or controls.

MCI、AD 患者或对照患者脑脊液中 ACE 活性。

基本信息

批准号：
17590591
负责人：
OHRUI Takashi
金额：
$ 1.92万
依托单位：
TOHOKU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

项目摘要

Little is known about the ACE activity in the CNS in living patients with AD. We therefore measured ACE activity in CSF in patients with mild cognitive impairment (MCI) and mild-to-moderate AD, and compared them with age-matched healthy controls. We also examined whether treatment by a brain-penetrating ACE inhibitor can alter CSF-ACE activity in patients with mild-to-moderate AD. The mean baseline MMSE value was 18.9 ± 0.7 (SE) in 付he AD group; 25.0 ± 0.4 in the MCI group; and 28.5 ± 0.3 in the normal group. CSF-ACE activity was elevated in the MCI group [0.32 (mean) ± 0.13 (SE) IU/L, n = 20] vs the control group (0.17 ± 0.02 IU/L, n = 20, p < 0.0001). There was also an increase in the mean CSF-ACE activity in the AD group (0.24 ± 0.01 IU/L, n = 34, p = 0.0219) vs the control group. The brain-penetrating ACE inhibitor, perindopril inhibited CSF-ACE activity in patients with AD after 1 month of treatment [0.24 ± 0.02 (before) vs 0.13 ± 0.03 IU/L (after), n = 7, p = 0.038]. There was no significant difference in the concentration of CSF somatostatin among the MCI, AD or control groups. We therefore assume that an increased CNS-ACE activity might be involved in the progression of AD, although the precise mechanism remains unknown. Brain-penetrating ACE inhibitor might provide a protection against progression of AD or MCI.

Little is known about the ACE activity in the CNS in living patients with AD. We therefore measured ACE activity in CSF in patients with mild cognitive impairment (MCI) and mild-to-moderate AD, and compared them with age-matched healthy controls. We also examined whether treatment by a brain-penetrating ACE inhibitor can alter CSF-ACE activity in patients with mild-to-moderate AD. The mean baseline MMSE value was 18.9 ± 0.7 (SE) in the AD group; 25.0 ± 0.4 in the MCI group; and 28.5 ± 0.3 in the normal group. CSF-ACE activity was elevated in the MCI group [0.32 (mean) ± 0.13 (SE) IU/L, n = 20] vs the control group (0.17 ± 0.02 IU/L, n = 20, p < 0.0001). There was also an increase in the mean CSF-ACE activity in the AD group (0.24 ± 0.01 IU/L, n = 34, p = 0.0219) vs the control group. The brain-penetrating ACE inhibitor, perindopril inhibited CSF-ACE activity in patients with AD after 1 month of treatment [0.24 ± 0.02 (before) vs 0.13 ± 0.03 IU/L (after), n = 7, p = 0.038]. There was no significant difference in the concentration of CSF somatostatin among the MCI, AD or control groups. We therefore assume that an increased CNS-ACE activity might be involved in the progression of AD, although the precise mechanism remains unknown. Brain-penetrating ACE inhibitor might provide a protection against progression of AD or MCI.