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Elsevier is the world's leading publisher of Medical Information. We are proud to make available our Patient Research option as a Beta program for patients, or friends/family of patients, who have a medical need for information regarding a medical situation for them or someone they know. This Beta program provides the article you request for free, with a small handling fee, $4.95. After ordering the article and confirmation of payment, we will e-mail the document to you typically within 2 hours, but no longer than 24 hours. A metabolic link between S-adenosylhomocysteine and polyunsaturated fatty acid metabolism in Alzheimer's disease Neurobiology of Aging, Volume 28, Issue 12, December 2007, Pages 1834-1839 Abstract: There is evidence that vascular risk factors contribute to the pathology of Alzheimer's disease. Increased concentrations of circulating homocysteine are associated with vascular risk factors and Alzheimer's disease but the mechanisms involved are unclear. Homocysteine inhibits the hydrolysis of S-adenosylhomocysteine (SAH) which is a product inhibitor of S-adenosylmethionine (SAM) dependent methyltransferase reactions. It has been shown previously that SAH inhibits phosphatidylethanolamine N-methyltransferase (PEMT) in the liver. The activity of PEMT in the liver plays an important role in the methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) and the delivery of essential polyunsaturated fatty acids (PUFAs) to peripheral tissues. In the present study, the plasma concentrations of SAH, SAM and homocysteine and the erythrocyte composition of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and their respective polyunsaturated fatty acid concentrations were determined in 26 patients with Alzheimer's disease and compared to those in 29 healthy control subjects. There was a significant increase in the plasma concentrations of SAH (p<0.001) and homocysteine (p<0.001) and a significant increase in the plasma concentrations of SAM (p<0.001) in the Alzheimer's patients. A significant positive correlation was found between the plasma concentrations of SAH and homocysteine (r=0.738, p<0.001). There was a negative correlation between the plasma concentrations of homocysteine and the ratio of SAM/SAH (r=−0.637, p<0.01). There was a significant decrease in the erythrocyte content of PC (p<0.001) and an increase in the erythrocyte content of PE (p<0.001) in the Alzheimer's patients. Plasma SAH concentrations were negatively related to erythrocyte PC concentrations (r=−0.286, p<0.01) and positively related to erythrocyte PE concentrations (r=0.429, p<0.001). The erythrocyte PC from Alzheimer's patients had a significant depletion of docosahexaenoic acid (DHA) (p<0.001) while there was no significant difference in the DHA content of erythrocyte PE. There was a significant negative correlation between plasma SAH and the DHA composition of erythrocyte PC (r=−0.271, p<0.001). This data may reflect the inhibition of hepatic PEMT activity by SAH in Alzheimer's disease. The decreased mobilization of DHA from the liver into plasma and peripheral tissues may increases the risk of atherosclerosis and stroke leading to chronic cerebral hypoperfusion. The evidence suggests that a metabolic link between the increased production of SAH and phospholipid metabolism may contribute to cerebrovascular and neurodegenerative changes in Alzheimer's disease. This Beta program is not intended for use by Medical Professionals. To obtain this document through the Patient Research option you must have a medical need, only use the document for personal use, and agree to all the terms and conditions below. Also, these articles can be obtained for free at your local public or university hospital library. We encourage you to use this as a means of obtaining articles of interest to you. Patient Research Terms and Conditions The terms and conditions set out below govern your use of the content made available through this web-site (the "Site"), including the article or articles that you have selected in connection with your personal medical research (the "Content") for delivery to the e-mail address you will be asked to provide in connection with this service (collectively, the "Service"). In order to provide this Service you understand and agree to provide the personal information you will be asked to provide after you accept these terms and conditions, although our use of such information will be limited to this purpose and otherwise governed by our privacy policy (see Privacy Policy). The Content, the Site and the Service are provided by Elsevier Inc. and its affiliates and licensors (collectively "Elsevier"). For further information about Elsevier or to contact us, see Contact Us. 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