Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apolipoprotein mimetic peptides dramatically reduce atherosclerosis in animal models, and may be an excellent mode of therapy to treat a variety of vascular inflammatory conditions, including atherosclerosis. Studies of apolipoprotein mimetic peptides in models of inflammatory disorders other than atherosclerosis, including viral influenza, asthma, chronic rejection after heart transplantation, sickle cell disease, scleroderma, diabetes, cognitive dysfunction and renal inflammation, suggest that apolipoprotein mimetic peptides may have efficacy in a wide range of inflammatory conditions.
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PMID:Multiple indications for anti-inflammatory apolipoprotein mimetic peptides. 1895 Dec 94

As a marker of generalized atherosclerosis, peripheral arterial disease (PAD) has implications not only for the affected lower extremity but also to overall cardiovascular health. It confers an increased risk of non-fatal and fatal vascular events which increases with the severity of the disease. Patient-based studies have shown that individuals with advanced PAD tend to perform poorly on cognitive tests compared to controls. In population studies, PAD is associated with an increased cognitive decline independently of previous cerebrovascular disease and cardiovascular risk factors. A low ankle-brachial index (ABI) may be an early predictor of cognitive decline and of potential value in identifying individuals at increased risk of cognitive impairment. In patients with PAD, secondary preventive measures directed at decreasing the long-term systemic vascular complications may also be important to the preservation of cognitive health. However, evidence suggests that PAD patients may be undertreated with regard to atherosclerotic risk factors, as demonstrated by an undue emphasis on symptom relief rather than essential risk factor reduction. More research needs to be carried out to determine the predictors of cognitive function in PAD patients, whether subtle cognitive disturbances are related to activities of daily living, including medical treatment compliance, and whether neuroprotective strategies and atherosclerotic risk factor control positively influence cognitive function in these high-risk patients.
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PMID:Peripheral arterial disease and cognitive function. 1914 80

HIV-associated hypogonadism is known to be a prevalent endocrine disorder, with a multifactorial etiology. Low testosterone levels are associated with decreased muscle mass, exercise capacity loss, erectile dysfunction, cognitive impairment, depression and decreased quality of life. In the same way, hypogonadism in HIV-infected men is associated with decreased muscle mass quantity and function, changes in corporal fat mass distribution and quantity, secretion of adipocytokines and endothelial dysfunction. This combined effect renders the entire body less sensitive to insulin, promoting development of atherosclerosis and glucose metabolism disorders. The clinical presentation is non-specific and hypogonadism screening scales are not useful in this population. Diagnostic procedures must include determination of free testosterone (FTc) in any HIV-infected men at the time of first HIV diagnosis and periodically, because of the clinical implications and the absence of specific predictive disease factors. Substitutive hormonal treatment must be offered only for HIV-infected men with FTc under reference levels and when reversible causes have been ruled out. Metabolic impact of hypogonadism suggests the incorporation of low testosterone levels to the list of cardiovascular risk factor in HIV-infected men.
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PMID:[Hypogonadism, erectile dysfunction and endothelial dysfunction among HIV-infected men]. 2193 92

Hypercholesterolemia increases the risk for dementia. Some studies suggest that statins may protect cognition, but findings are conflicting. Unmeasured confounders, including high-density lipoprotein (HDL) cholesterol or subclinical atherosclerosis, may have influenced prior study outcomes. In older adults participating in a population-based cohort study (n=1711, aged 65 to 97 y), we investigated the relationships of total and HDL cholesterol levels, statin use, and carotid intima-media thickness with the prevalence of cognitive impairment. In adjusted models, participants in the highest quartile of non-HDL (total-HDL) cholesterol had an increased odds of cognitive impairment compared with those in the lowest quartile [odds ratio (OR): 2.06, 95% confidence interval (CI): 1.07-3.98]. Statin use was associated with lower odds of cognitive impairment in unadjusted models (OR: 0.57, 95% CI: 0.36-0.89), but this relationship was not significant after adjusting for vascular and lifestyle factors (OR: 0.84, 95% CI: 0.47-1.49). In this analysis of older adults, increased atherogenic lipoproteins were associated with impaired cognition. Statin use was related to many factors that both negatively and positively affect cognition, but was not associated with better cognitive function. These results suggest that confounding by indication may explain the contradictory findings in studies assessing the association of statins with cognition. Randomized-controlled clinical trials and longitudinal studies are necessary to determine if statins protect against cognitive decline.
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PMID:Increased atherogenic lipoproteins are associated with cognitive impairment: effects of statins and subclinical atherosclerosis. 1993 44

Vascular cognitive impairment is an important cause of cognitive decline in the elderly. Ischemic lesions in the brain have an influence on the natural history of dementia. Vascular dementia can be caused by small-vessels disease (S-VaD) or by large-artery atherosclerosis with vascular lesions in strategic areas of the brain (M-VaD). In both cases changes in white matter are observed. In 60 patients with S-VaD and in 34 with M-VaD the presence of vascular and biochemical risk factors was evaluated and compared to age and sex matched 126 controls without dementia. Coronary artery disease, atrial fibrillation, hypertension and strokes were observed more frequently in both investigated groups. Of biochemical risk factors, hyperhomocysteinemia (associated with low levels of folic acid and vitamin B 12) and low HDL cholesterol levels were found in both forms of VaD.
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PMID:Vascular and biochemical risk factors of vascular dementia after lacunar strokes (S-VaD) and after multiinfarcts in strategic areas (M-VaD). 1933 23

Drugs currently used in the treatment of cognitive impairment and dementia have a very limited therapeutic value, suggesting the necessity to potentially individualize new strategies able to prevent and to slow down the progression of predementia and dementia syndromes. An increasing body of epidemiological evidence suggested that elevated saturated fatty acids (SFA) could have negative effects on age-related cognitive decline (ARCD) and mild cognitive impairment (MCI). Furthermore, a clear reduction of risk for cognitive decline has been found in population samples with elevated fish consumption, high intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), particularly n-3 PUFA. Epidemiological findings demonstrated that high PUFA intake appeared to have borderline non-significant trend for a protective effect against the development of MCI. Several hypotheses could explain the association between dietary unsaturated fatty acids and cognitive functioning, including mechanisms through the co-presence of antioxidant compounds in food groups rich in fatty acids, via atherosclerosis and thrombosis, inflammation, accumulation of b-amyloid, or via an effect in maintaining the structural integrity of neuronal membranes, determining the fluidity of synaptosomal membranes that thereby regulate neuronal transmission. However, recent findings from clinical trials with n-3 PUFA supplementation showed efficacy on depressive symptoms only in non-apolipoprotein E (APOE) epsilon4 carriers, and on cognitive symptoms only in very mild Alzheimer's disease (AD) subgroups, MCI patients, and cognitively unimpaired subjects non-APOE epsilon4 carriers. These data together with epidemiological evidence support a possible role of fatty acid intake in maintaining adequate cognitive functioning and possibly for the prevention and management of cognitive decline and dementia, but not when the AD process has already taken over.
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PMID:Dietary fatty acids in dementia and predementia syndromes: epidemiological evidence and possible underlying mechanisms. 1964 7

The ankle-brachial index (ABI), a marker of generalized atherosclerosis, is related to cognitive impairment in older adults. We investigated whether ABI is associated specifically with age-related cognitive decline. We measured ABI at recruitment and 5 and 12 years later in a sample of individuals aged 55-74 years. Cognition was measured in 717 of these participants 10 years after recruitment and 5 years later. It was found that ABI was associated with the level of cognitive function, even after adjustment for estimated premorbid function and concurrently measured anxiety and depression (standardized coefficient of 0.07), but this was attenuated by anxiety and depression. ABI was not associated with change in cognitive function. In conclusion, over long time periods, low ABI may be associated with reduced cognitive function in older adults, at least partly because the associated poor health creates anxiety and depression.
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PMID:Ankle--brachial index predicts level of, but not change in, cognitive function: the Edinburgh Artery Study at the 15-year follow-up. 2014 79

The essentiality of zinc was recognized 46 years ago. Zinc deficiency resulting in growth retardation, hypogonadism, immune dysfunction and cognitive impairment affects nearly 2 billion subjects in the developing world. High phytate content of the cereal proteins consumed in the developing world, results in decreased availability of zinc for absorption. Zinc therapy has been very successful and life saving measure in patients with acrodermatitis enteropathica and Wilson's disease. Beneficial therapeutic responses of zinc supplementation have been ovserved in acute diarrhea in children, chronic hepatitis C, shigellosis, leprosy, leishmaniasis, and common cold. Zinc supplementation was effective in decreasing incidences of infection in elderly and patients with sickle cell disease. Zinc supplementation was effective in preventing blindness in 25% of the elderly with dry type of age related macular degeneration. Zinc supplementation in the elderly decreased oxidative stress and decreased generation of inflammatory cytokines. Zinc is an intracellular signaling molecule in monocytes, dendritic cells and macrophages and it plays an important role in cell-mediated immune functions and oxidative stress. Zinc is also an anti-inflammatory agent. These unique properties of zinc may have significant therapeutic benefits in several diseases in humans. In many diseases concurrent zinc deficiency may complicate the clinical features, affect adversely immunological status, increase oxidative stress and increase generation of inflammatory cytokines. Oxidative stress and chronic inflammation may play important causative roles in many chronic diseases, including atherosclerosis, several malignancies, neurological disorders, and auto-immune diseases. It is therefore, important that status of zinc is assessed and zinc deficiency corrected in these chronic diseases. A controlled clinical trial of zinc supplementation in these disorders in order to document the preventive and therapeutic effects of zinc is warranted.
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PMID:Impact of the discovery of human zinc deficiency on health. 2015 May 99

The vascular hypothesis of Alzheimer's disease (AD) which we first proposed in 1993, has become a useful concept in identifying vascular risk factors for AD or vascular dementia that can be modified through appropriate treatment to prevent, reduce or delay the onset of cognitive impairment and dementia onset. Among the more than two dozen vascular risk factors already identified for AD, are cardiovascular disease and carotid artery atherosclerosis, which may exert their pathology by chronically lowering cerebral hypoperfusion during aging. We propose and plan to initiate a clinical study to screen middle-aged, cognitively intact individuals, with carotid artery ultrasound and echocardiography to identify potentially progressive pathology in the heart and carotid artery that is considered modifiable with optimal medical treatment. This clinical strategy, if found effective in preventing pathologic conditions suspected of contributing to severe cognitive impairment, could significantly reduce AD prevalence if applied on a wide scale and help promote healthier mental and physical aging while providing a compelling economic benefit to society.
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PMID:The vascular hypothesis of Alzheimer's disease: bench to bedside and beyond. 2017 40

The relationship between cerebrovascular impairment and Alzheimer's disease is a controversial debate. An important and topical aspect in clinical research is the attempt to define the role of atherosclerosis and its determinants in the presentation and evolution of dementia. In this article, we discuss the evidence of the interaction between degenerative and vascular mechanisms in the pathogenesis of dementia. Moreover, we present data about the influence of hypertension and dyslipidemia, usually considered among the most important risk factors for atherosclerosis, on the evolution of Alzheimer's disease. The effects of antihypertensive and lipid-lowering drugs on cognitive impairment will be also discussed.
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PMID:Atherosclerosis in the evolution of Alzheimer's disease: can treatment reduce cognitive decline? 2018 31


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