کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9016699 | 1128110 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The central nervous system in animal models of hyperhomocysteinemia
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کلمات کلیدی
5-HTDOPACNMDAMPTP5-HIAAGLUT-1CBSeNOSSAHTBARSHCAGADN-methyl d-aspartateMTHFRSAMVCAM-1S-adenosylhomocysteineNSEDZA3,4-dihydroxyphenylacetic acid - 3،4-دی هیدروکسی فنیل اسیدهای اسیدneuron specific enolase - enolase خاص نورونglutamic acid decarboxylase - glutamic acid dearboxylaseApoe - آپوapolipoprotein E - آپولیپوپروتئین ES-adenosylmethionine - اس-ادنوزیل متیونینSchizophrenia - اسکیزوفرنی یا شیزوفرنیHomocysteic acid - اسید هوموسیستیکHomovanilic acid - اسید هومیانیلیکAlzheimer's disease - بیماری آلزایمرCerebrovascular disease - بیماری عروق مغزیNutrition - تغذیهtHcy - تیسیDementia - جنون یا زوال عقلSerotonin - سروتونینendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالStroke - سکته مغزیFolate - فولاتmethylene tetrahydrofolate reductase - متیلن تتراهیدروفلوات ردوکتازMethionine - متیونینAnimal models - مدل های حیوانیthiobarbituric acid reactive substances - مواد واکنش پذیر اسید تیوباربیتوریکvascular cell adhesion molecule-1 - مولکول چسبندگی سلولی عروقی-1Glucose transporter Type 1 - نوع گلوکز 1 نوعPlasma total homocysteine - هموسیستئین کل پلاسماhomocysteine - هوموسیستئینHVA - چه
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
روانپزشکی بیولوژیکی
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چکیده انگلیسی
Growing epidemiological evidence of associations between mildly elevated plasma homocysteine with age-related cognitive impairment, neurodegenerative and cerebrovascular disease has stimulated interest in the role of homocysteine in neurological and neuropsychiatric disorders. Homocysteine is an intermediate in the folate, vitamin B12 and B6 dependent pathways of one-carbon and sulfur amino acid metabolism. Impairments of these pathways may cause CNS dysfunction by promoting the intracellular generation of homocysteine, which is postulated to have vasotoxic and neurotoxic properties. It might also inhibit the methylation of myelin basic protein and membrane phospholipids, or disrupt biogenic amine metabolism and many other vital CNS reactions. However, it is unclear which, if any, of these putative mechanisms underlies the epidemiological associations. Genetic mouse models of hyperhomocysteinemia suggest that the primary metabolic disturbances rather than homocysteine per se may be important in determining neurological outcomes. However, severe and early developmental abnormalities in these mice limit their usefulness for understanding the relation of hyperhomocysteinemia to adult CNS disorders. Pharmacologic and dietary studies on homocysteine in rodents have reported heightened neuronal sensitivity to neurotoxic insults, neurochemical abnormalities and cerebrovascular dysfunction. Such studies are consistent with a causal relationship, but they fail to distinguish between effects that might result from a dietary imbalance and those that might be caused by homocysteine per se. Future work should be directed towards refining these models in order to distinguish between the effects of homocysteine and its determinants on neurological and behavioral outcomes that represent different CNS disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 29, Issue 7, September 2005, Pages 1140-1151
Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 29, Issue 7, September 2005, Pages 1140-1151
نویسندگان
Aron M. Troen,