Bär Karl-Jürgen, Boettger Michael Karl, Seidler Nicole, Mentzel Hans Joachim, Terborg Christoph, Sauer Heinrich
Department of Psychiatry, Friedrich-Schiller-University Jena, Philosophenweg 3, 07743 Jena, Germany.
Stroke. 2007 Dec;38(12):3186-92. doi: 10.1161/STROKEAHA.107.492033. Epub 2007 Oct 25.
Recent reports suggest that vascular factors play a crucial role in the development and progression of Alzheimer's disease. We aimed to assess vasomotor reactivity in patients with Alzheimer's disease and vascular dementia due to microangiopathy using transcranial Doppler sonography and near-infrared spectroscopy during a CO(2) exposition task.
The normalized CO(2) reactivity assessed at the middle cerebral artery and the oxygenated and deoxygenated hemoglobin of the frontal cortex were obtained. To investigate the impact of cholinergic deficiency known for Alzheimer's disease on vasomotor reactivity, both groups were reinvestigated during treatment with the acetylcholine esterase inhibitor galantamine.
Transcranial Doppler analysis revealed significantly reduced normalized CO(2) reactivity for Alzheimer's disease and vascular dementia. Vasomotor reactivity assessed by near-infrared spectroscopy was decreased in patients with vascular dementia, but not in Alzheimer's disease. Galantamine treatment showed a beneficial effect, normalizing these parameters close to age-matched control levels.
Our results suggest that Alzheimer's disease is associated with a lack of vasomotor reactivity, which might be associated with disturbed autoregulation indicating a potential risk for a decreased protection of brain tissue against blood pressure changes. Additionally, a diminished increase of cortical oxygenated hemoglobin during the CO(2) test was apparent in patients with vascular dementia. Galantamine treatment influenced vascular reactivity in the CO(2) test, thus providing evidence for the cholinergic deficiency, thereby adding to vascular dysregulation in Alzheimer's disease, but also indicating an important role of cholinergic system dysfunction for vascular dementia.
近期报告表明,血管因素在阿尔茨海默病的发生和发展中起着关键作用。我们旨在通过经颅多普勒超声和近红外光谱技术,在二氧化碳暴露试验中评估阿尔茨海默病患者以及因微血管病变导致的血管性痴呆患者的血管运动反应性。
获取大脑中动脉处评估的标准化二氧化碳反应性以及额叶皮质的氧合血红蛋白和脱氧血红蛋白。为研究阿尔茨海默病中已知的胆碱能缺乏对血管运动反应性的影响,两组患者在接受乙酰胆碱酯酶抑制剂加兰他敏治疗期间再次接受检查。
经颅多普勒分析显示,阿尔茨海默病和血管性痴呆患者的标准化二氧化碳反应性显著降低。通过近红外光谱评估的血管运动反应性在血管性痴呆患者中降低,但在阿尔茨海默病患者中未降低。加兰他敏治疗显示出有益效果,使这些参数接近年龄匹配的对照水平。
我们的结果表明,阿尔茨海默病与血管运动反应性缺乏有关,这可能与自身调节紊乱有关,提示脑组织对血压变化的保护作用降低存在潜在风险。此外,在二氧化碳试验期间,血管性痴呆患者皮质氧合血红蛋白的增加明显减少。加兰他敏治疗影响了二氧化碳试验中的血管反应性,从而为胆碱能缺乏提供了证据,这不仅增加了阿尔茨海默病中的血管调节异常,也表明胆碱能系统功能障碍在血管性痴呆中起重要作用。