Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Weight loss is a nutritional problem commonly associated with Alzheimer disease. Two types of weight loss have been described. A severe weight loss correlated with a decrease in daily caloric intake and with increased difficulties in performing the activities of daily living. A slowly progressive but clinically significant loss, not associated with either a decrease in caloric intake or an inflammatory syndrome. It is difficult to explain this type of weight loss as subjects have adequate caloric intakes. Several hypothesis are however considered as increased energy requirements (which can result from increased energy expenditure, from increased metabolic disorder, or from increased growth hormone secretion), or mesial temporal cortex atrophy. But, at the present time, no study can give a proper explanation. Vitamin deficiencies, specially vitamin B6, B12 and folates, high homocysteine level, antioxidants deficiencies (especially, vitamin E deficiency), iron, counter, and phenol derived could also influence the memory capacities and have an effect upon cognitive impairment, as reported in epidemiological studies. The prevention of nutritional deficiencies in patients with Alzheimer's disease, could be one of the strategies to improve the caregiver and the patients quality of life.
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PMID:[Alzheimer's disease and nutrition]. 1042 97

Lipoproteins modified by oxidation, glycation, alkylation, and nitration are generated by oxidative stress during inflammation, diabetes, and inadequate supply of dietary antioxidants. A family of genes, the scavenger receptors, recognizes and internalizes modified lipoproteins, making them susceptible to degradation. Clearance of modified lipoproteins by scavenger receptors occurs mainly in macrophages, dendritic cells, and Kupffer cells of the liver. However, scavenger receptor expression also occurs in other cells, such as endothelial cells, aortic smooth muscle cells, neuronal cells, and keratinocytes. Thus, the local clearance of oxidized low-density lipoprotein and the resolution of inflammatory processes may rely in part on the expression of scavenger receptors in "nonprofessional" phagocytes. Uptake of oxidized low-density lipoprotein, without an efficient machinery to degrade them and uncontrolled expression of scavenger receptors, may lead to cellular deregulation, apoptosis, and formation of foam cells. Diseases accompanied by oxidation of lipoproteins, such as atherosclerosis, Alzheimer disease, glomerulosclerosis, ataxia with vitamin E deficiency, and possibly age-dependent lipofuscin deposition, may share a common pathogenetic feature. This review will focus on foam cell formation, mainly within the atherosclerotic lesion, and the possible involvement of aberrant regulation of the scavenger receptor genes. To date, the regulatory mechanisms at the basis of scavenger receptor gene expression and their roles in atherosclerosis and other diseases are not well established. Knowledge on this subject could lead to a better understanding of the pathogenesis, prevention, and therapy of these diseases.
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PMID:Scavenger receptors and modified lipoproteins: fatal attractions? 1090 71

Brain because of its functions, is isolated from either external or internal environment. This function is performed by skull, cerebral meninges, cerebrospinal fluid and unique system of mechanisms and barriers restricting exchange of oxygen, soluble substances between blood, nervous tissue and cerebrospinal fluid. Mato cells, located in Virchow-Robin's space play a key role in blood-brain barrier. Mato cells are rich in hydrolytic enzymes. They act as phagocytes in blood-brain barrier by scavenger receptors, which take part in eliminating excess of unfavorable substances from environment. Ageing, hypercholesterolemia and vitamin E deficiency can cause degeneration of perivascular cells and limit their protective function. Mato cells probably are responsible for pathogenesis of various diseases, f.e. Alzheimer disease, diabetic rethinopathy, encephalitis.
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PMID:[Blood-brain barrier--function of Mato cells]. 1965 Apr 32