[Prevention of vascular dementia. Evidence and practice].
ABSTRACT During recent years, increasing knowledge has been obtained from clinical studies about the impact that vascular factors have on cognitive function and dementia. Due to demographic reasons and still insufficient control of all vascular risk factors, dementia and associated problems are of increasing importance and will have impact on economical and social development in most countries. The incidence of cognitive impairment and dementia will increase exponentially. As long as no causal therapy for dementia exists, diagnosis and control of risk factors for dementia will need much more attention. Hypertension is not only the most important risk factor for stroke that often leads to dementia but also for silent brain infarcts, which are also associated with onset of dementia. Uncontrolled hypertension is associated with cognitive impairment and sufficient control of hypertension in middle-aged patients can reduce the risk of dementia in older ages. Nevertheless, treatment of all other risk factors (e.g., diabetes mellitus, hyperlipidemia, atrial fibrillation) is important to reduce the onset of not only vascular but also Alzheimer dementia.
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ABSTRACT: We conducted a cross-sectional epidemiological survey using ambulatory blood pressure monitoring and brain MRI in a cohort from northern Japan to determine whether an inappropriately low nocturnal blood pressure, or an excess fall in nocturnal blood pressure, might be responsible for silent cerebrovascular lesions in the elderly. Untreated subjects over 55 years and under 64 years of age (late middle age; 24 men and 46 women, 60% of eligible people) and over 65 years and under 75 years of age (elderly; 29 men and 52 women, 91% of eligible people) participated in the study. We evaluated the relationship between the amplitude (Daytime Average-Nighttime Average) or the rate ([Daytime Average-Nighttime Average]/Daytime Average) of the fall in nocturnal blood pressure and the incidence of silent cerebrovascular lesions on MRI (number of lacunar infarctions or extent of periventricular hyperintensity). The amplitude or the rate of the fall in nocturnal blood pressure in elderly women with one or two lacunar infarctions was significantly higher than that in those without such infarctions. There was a significant positive correlation between the amplitude or the rate of the fall in nocturnal blood pressure and the extent of periventricular hyperintensity in the elderly women. This relationship was observed in women, but not in men, of late middle age; this was not seen in elderly men. Results indicate that an inappropriately low nocturnal blood pressure, or an excessive fall in nocturnal blood pressure, is associated with ischemic silent cerebrovascular lesions, at least in elderly women. Treatment of hypertension in such women should be administered with care and with regard to nocturnal blood pressure.Stroke 09/1996; 27(8):1319-27. · 6.16 Impact Factor
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ABSTRACT: Vascular causes of dementia may be more common than supposed. Vascular factors may also have a role in late-onset Alzheimer's disease, but the role of hypertension in the development of dementia is unclear. As part of the Longitudinal Population Study of 70-year-olds in Göteborg, Sweden, we analysed the relation between blood pressure and the development of dementia in the age intervals 70-75, 75-79, and 79-85 years in those non-demented at age 70 (n = 382). The sample was followed up for 15 years and examined repeatedly with a comprehensive investigation, including a psychiatric and physical examination. a Participants who developed dementia at age 79-85 had higher systolic blood pressure at age 70 (mean 178 vs 164 mm Hg, p = 0.034) and higher diastolic blood pressure at ages 70 (101 vs 92, p = 0.004) and 75 (97 vs 90, p = 0.022) than those who did not develop dementia. For subtypes of dementia, higher diastolic blood pressure was recorded at age 70 (101, p = 0.019) for those developing Alzheimer's disease and at age 75 (101, p = 0.015) for those developing vascular dementia than for those who did not develop dementia. Participants with white-matter lesions on computed tomography at age 85 had higher blood pressure at age 70 than those without such lesions. Blood pressure declined in the years before dementia onset and was then similar to or lower than that in non-demented individuals. Previously increased blood pressure may increase the risk for dementia by inducing small-vessel disease and white-matter lesions. To what extent the decline in blood pressure before dementia onset is a consequence or a cause of the brain disease remains to be elucidated.The Lancet 05/1996; 347(9009):1141-5. · 39.06 Impact Factor
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ABSTRACT: We examined the possibility that continuous activation of the human brain renin-angiotensin system causes cognitive impairment, using human renin (hRN) and human angiotensinogen (hANG) gene chimeric transgenic (Tg) mice. Cognitive function was evaluated by the shuttle avoidance test once a week from 10 to 20 weeks of age. The avoidance rate in wild-type mice gradually increased. In contrast, the avoidance rate in chimeric hRN/hANG-Tg mice also increased; however, no further increase in avoidance rate was observed from 14 weeks of age, and it decreased thereafter. Cerebral surface blood flow was markedly reduced in 20-week-old hRN/hANG-Tg mice. Superoxide anion production in the brain was already higher in 10-week-old hRN/hANG-Tg mice and further increased thereafter with an increase in NADPH oxidase activity. Moreover, expression of p47(phox) and Nox4 in the brain of hRN/hANG-Tg mice also increased. Administration of an angiotensin II type 1 receptor blocker, olmesartan (5.0 mg/kg per day), attenuated the increase in blood pressure and ameliorated cognitive decline with enhancement of cerebral surface blood flow and a reduction of oxidative stress in hRN/hANG-Tg mice. On the other hand, hydralazine (0.5 mg/kg per day) did not improve the decrease in avoidance rate, and did not influence cerebral surface blood flow or oxidative stress in hRN/hANG-Tg mice, in spite of a similar reduction of blood pressure to that by olmesartan. Moreover, we observed that treatment with Tempol improved impaired cognitive function in hRN/hANG-Tg mice. These results suggest that continuous activation of the brain renin-angiotensin system impairs cognitive function via stimulation of the angiotensin II type 1 receptor with a decrease in cerebral surface blood flow and an increase in oxidative stress.Hypertension 01/2009; 53(2):356-62. · 6.87 Impact Factor