Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apolipoprotein (apo) E plays an important role in lipid metabolism, and the major isoforms of apoE (apoE2, apoE3, and apoE4) have significantly different metabolic effects. Apolipoprotein E4 is associated with a higher risk of both heart disease and Alzheimer's disease (AD). Patients homozygous for apolipoprotein E2 are predisposed to type III hyperlipoproteinemia, and apoE2 may be protective against AD. Structure/function studies have proved to be a useful tool in understanding how the different apoE isoforms result in different pathological consequences. As these studies continue, it is essential to have a reliable method to produce large quantities of apoE and mutants of apoE. We describe here a method of apoE production in Escherichia coli strain BL21(DE3). The cDNA from apoE isoforms was inserted into a pET32a vector with a T7 promoter and a fusion partner (thioredoxin). The T7 promoter results in high expression of an easily purified His-tagged fusion protein. A thrombin recognition site was positioned in the expression vector so that only two novel amino acids (Gly-Ser) are added to the amino terminus of apoE following the removal of thioredoxin. Approximately 20 mg of apoE is obtained from a 1-liter culture. The major isoforms of apoE produced with this system were extensively characterized for their ability to bind the low-density lipoprotein (LDL) receptor, for their characteristic lipid association preferences, and for their stability as measured by guanidine denaturation. The recombinant proteins behaved identically to plasma-derived apoE isoforms.
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PMID:Functional characterization of apolipoprotein E isoforms overexpressed in Escherichia coli. 1041 18

Although epidemiological studies are limited by diagnostic uncertainties, they suggest that stroke increases the risk of dementia. The mortality rate is higher in vascular dementia (VaD) than in Alzheimer's disease (AD). Community-based studies have provided several consistent findings: (i) age dependence with prevalence rates doubling every 5 years, (ii) a higher frequency in men and (iii) nation-to-nation differences. The prevalence of VaD ranges from 2.2% in 70- to 79-year-old women, to 16.3% in men >80 years. One sixth of acute stroke patients have preexisting dementia. The incidence of VaD has been studied much less extensively than that of AD, and substantial variations in the incidence rates have been observed: annual incidence rates (per 100,000) range from 20 to 40 between 60 and 69 years of age and from 200 to 700 over 80. The incidence rate of VaD declined over the last 2 decades, probably as a consequence of effective stroke prevention. It is generally assumed that risk factors for VaD are those of stroke, with arterial hypertension as leading factor, followed by atherosclerotic disease, low education level, alcohol abuse and heart disease. Stroke characteristics, such as lacunar infarction and left-sided hemispheric lesions, are major determinants of VaD. The cerebrovascular lesions are likely to be the only cause of dementia in strategic infarcts, in lacunar state, in hereditary cystatin C amyloid angiopathy and in CADASIL. However, white matter changes, and associated Alzheimer pathology, which are both frequent in this age category, may also contribute to the cognitive decline.
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PMID:Epidemiology of vascular dementia. 1042 61

Vascular dementia (VD) is more prevalent than Alzheimer's disease (AD) in Japan, while AD is more common in Western countries. In the Hisayama study, a community-based cohort study of Japan, the prevalence of VD decreased in men during the 7-years (1985-1992) follow-up period, while the prevalence of AD remained unchanged both in men and women. The incidence of dementia increases with age, particularly AD aged 85 or older. Hypertension is a major risk factor for VD. Other risk factors include age, prior stroke, diabetes, alcohol intake, heart disease, and smoking. In contrast, age, a family history of dementia, a low educational level, and low physical activity are risk factors for AD. The role of hypertension in AD remains controversial; there has been positive, negative, or no association existed between blood pressure levels and AD. A recent clinical trial has disclosed the potential preventive effect of antihypertensive treatment on the incidence of dementia, especially of AD. Although the role of vascular factors for the pathogenesis of AD is becoming recognized, the effectiveness of antihypertensive treatment on the prevention of AD should be further clarified in the future studies.
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PMID:Hypertension and dementia. 1042 14

Depression is a significant concern in elderly patients. Reported prevalence rates differ greatly depending on the definition of depression and the population of interest, with increases reported in settings where comorbid physical illnesses are more common. In community-dwelling elderly patients, prevalences of depressive symptoms and major depressive disorder are 15% and 1% to 3%, respectively. Factors associated with depression in the elderly include female gender, alcohol and substance abuse, pharmaceuticals, family history, and medical conditions such as stroke, Alzheimer's disease, cancer, and heart disease. Recognition of depression is complex because patients often deny their depression, present with somatic complaints, or may have comorbid anxiety or cognitive impairment. Depression is underrecognized and undertreated in the elderly, despite evidence that the benefits of treatment outweigh potential risks.
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PMID:Epidemiology and diagnosis of depression in late life. 1051 52

This essay considers the consequences of childhood experiences with family illness on future adult sensibilities. Novelist and memoirist Mary Gordon describes her father's early death from heart disease and her childhood responsibilities toward her mother who was chronically ill with polio. She examines the relations between the ill body and the rituals and teachings of Catholicism and, by implication, all religious imagings of the body. By detailing her current caregiving responsibilities toward her mother, who is now homebound with Alzheimer disease, she scrutinizes the responses of the healthy toward the ill. She cites passages from her own novels--The Other Side, The Shadow Man, and Spending--in which characters' bodies fail and sicken. By examining these retrospective and prospective experiences with other people's ailments, Gordon exhorts medical students and doctors to tend to the bodies in their care with skill, with vision, and with words. She joins fellow writer Joseph Conrad in his task: "by the power of the written word to make you hear, to make you feel; it is, before all, to make you see."
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PMID:Words, art, body and memory: readings from a writer. 1053 31

Today there are 78 million American baby boomers--persons between ages 35 and 53--comprising one-third of the U.S. population. According to psychologist and entrepreneur Ken Dychtwald, PhD, the 20th century has been ruled by the young, but the 21st century will belong to the "new-old." He predicts that as medical patients, the aging boomers will crave vigor, vitality, and life extension. The irony of past medical successes, he says, is that they have produced legions of long-lived elders who struggle with the very problems that the American health care system is ill-prepared to handle, such as heart disease, cancer, arthritis, osteoporosis, and Alzheimer's. The good news is that there are some solutions that Dr. Dychtwald believes could produce a healthier version of aging at a lower cost than today's system.
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PMID:'Age power': how the new-old will transform medicine in the 21st century. Interview by Alice V. Luddington. 1060 33

Feminist critiques of menopause have been beneficial in opening up important public health debates around menopause. One of the most contentious public health issues concerns the use of Hormone Replacement Therapy (HRT) for the prevention of osteoporosis, heart disease and, more recently, Alzheimer's disease, in postmenopausal women. For preventive purposes, it is recommended that women should take HRT for 10-15 years and preferably remain on the therapy for the remainder of their lives. This is despite reported increased cancer risks associated with HRT, side effects and considerable cost of the therapy. Various studies have shown that up to 50% of women stop taking HRT after 9-12 months. These figures are used in the medical literature as an indication of women's non-compliance. Extending earlier feminist critiques around menopause and HRT, this paper discusses a critical feminist engagement around issues of women's perceived non-compliance with HRT.
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PMID:Managing menopause: a critical feminist engagement. 1072 70

Factors accelerating cerebral degenerative changes represent potentially modifiable risks for cognitive decline. Putative risks accelerating subtle cognitive decline and dementia were correlated with repeated measures of cerebral atrophy, CT densitometry, perfusions, and cognitive testing among 224 neurologically and cognitively normative aging volunteers. After age 60, cerebral atrophy, ventricular enlargement, polioaraiosis, and leukoaraiosis geometrically increased as perfusions declined. Risks accelerating perfusional decline, cerebral atrophy, polioaraiosis, and leukoaraiosis were: transient ischemic attacks (TIAs), hypertension, smoking, hyperlipidemia, male gender. At age 71.5 +/- 11.9, subtle cognitive decline began, accelerated by TIAs, hypertension, and heart disease. Leukoaraiosis began before cognitive decline. TIAs, hypertension, and hyperlipidemia correlated with vascular dementias. Excessive cortical perfusional decreases and cerebral atrophy correlated with cognitive decline. Family history of neurodegenerative disease correlated with Alzheimer's disease. We concluded that TIAs, hypertension, hyperlipidemia, smoking, and male gender accelerate cerebral degenerative changes, cognitive decline, and dementia.
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PMID:Cardiovascular and other risk factors for Alzheimer's disease and vascular dementia. 1081 32

Putative risk factors accelerating mild cognitive decline and dementia were correlated with repeated measures of cerebral atrophy, CT, densitometry, perfusions, and cognitive testing among neurologically and cognitively normative aging volunteers. A total of 224 normative subjects at increased risk for cognitive decline were admitted to the study. Mean entry age was 59.5 +/- 15.8 years. Mean follow-up is 5.8 +/- 3.3 years. At follow-up, 22 developed mild cognitive impairment (41 CCSE >/= -3), 19 became demented-8 with Vascular type (VAD), 11 with Alzheimer's type (DAT)-and 183 remain cognitively unchanged. Cerebral atrophy, tissue densities, and perfusions were measured by Xe-CT. After age 60, cerebral atrophy, ventricular enlargement, and polio- and leuko-araiosis geometrically increased as perfusions declined. Risk factors accelerating perfusional decline, cerebral atrophy, polio-araiosis, and leuko-araiosis were: transient ischemic attacks (TIAs), hypertension, smoking, hyperlipidemia, and male gender. At age 71.5 +/- 11.9, mild cognitive impairment began accelerated by TIAs, hypertension and heart disease. Leuko-araiosis began before cognitive decline. TIAs, hypertension, and hyperlipidemia correlated with VAD. Excessive cortical perfusional decrease, gray and white matter hypodensities, and cerebral atrophy correlate with cognitive decline.
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PMID:Risk factors for cerebral hypoperfusion, mild cognitive impairment, and dementia. 1086 1

Increased prevalence of Alzheimer's disease-like beta-amyloid deposits in the neuropil and within neurons occurs in the brains of non-demented individuals with heart disease. Heart disease is a prevalent finding in Alzheimer's disease, and may be a forerunner to the dementing disorder. In the cholesterol-fed rabbit model of human coronary heart disease there is production and accumulation of beta-amyloid in the brain. This accumulation of beta-amyloid can be reversed by removing cholesterol from the rabbits' diet. In culture cells, a cholesterol challenge has been shown to increase production of beta-amyloid, and dramatic reductions of cholesterol produced by HMG Co-A reductase inhibitors decrease production of beta-amyloid. Increased beta-amyloid production is also produced by dietary cholesterol in a number of transgenic mouse models of Alzheimer's disease. Administration of HMG Co-A reductase inhibitors may block beta-amyloid production caused by dietary cholesterol in rabbits. Clinical trials testing the benefit of HMG Co-A reductase inhibitors in the treatment of Alzheimer's disease are underway.
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PMID:Link between heart disease, cholesterol, and Alzheimer's disease: a review. 1093 82


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