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Homocysteine concentrations in the cognitive progression of Alzheimer's disease
Brighton & Sussex Med Sch, Ctr Dementia Studies, Brighton BN1 9RY, E Sussex, England..
Univ Oxford, Dept Pharmacol, Oxford OX1 3QT, England.;Uppsala Univ, Dept Pharmaceut Biosci, S-75237 Uppsala, Sweden..
Univ Oxford, Dept Pharmacol, Oxford OX1 3QT, England..
Univ Surrey, Dept Nutrit Sci, Guildford GU2 7XH, Surrey, England..
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2017 (Engelska)Ingår i: Experimental Gerontology, ISSN 0531-5565, E-ISSN 1873-6815, Vol. 99, s. 146-150Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Objectives: Hyperhomocysteinemia in Alzheimer's disease (AD) is widely reported and appears to worsen as the disease progresses. While active dietary intervention with vitamins B12 and folate decreases homocysteine blood levels, with promising clinical outcomes in Mild Cognitive Impairment (MCI), this so far has not been replicated in established AD populations. The aim of the study is to explore the relationship between hyperhomocystenemia and relevant vitamins as the disease progresses. Methods: In this longitudinal cohort study, 38 participants with mild to moderate AD were followed for an average period of 13 months. Plasma folate, vitamin B12 and homocysteine concentrations were measured at baseline and at follow-up. Dietary intake of B vitamins was also measured. Spearman's correlations were conducted by homocysteine and B vitamin status. Results: As expected, cognitive status significantly declined over the follow-up period and this was paralleled by a significant increase in homocysteine concentrations (p = 0.006). However, during this follow-up period there was no significant decline in neither dietary intake, nor the corresponding blood concentrations of vitamin B12/folate, with both remaining within normal values. Changes in blood concentrations of B vitamins were not associated with changes in homocysteine levels (p > 0.05). Conclusion: In this study, the increase in homocysteine observed in AD patients as the disease progresses cannot be solely explained by dietary and blood levels of folate and vitamin B12. Other dietary and non-dietary factors may contribute to hyperhomocysteinemia and its toxic effect in AD, which needs to be explored to optimise timely intervention strategies.

Ort, förlag, år, upplaga, sidor
PERGAMON-ELSEVIER SCIENCE LTD , 2017. Vol. 99, s. 146-150
Nyckelord [en]
Homocysteine, B vitamins, Alzheimer's disease, Cognition
Nationell ämneskategori
Geriatrik
Identifikatorer
URN: urn:nbn:se:uu:diva-343562DOI: 10.1016/j.exger.2017.10.008ISI: 000415591300019PubMedID: 29024723OAI: oai:DiVA.org:uu-343562DiVA, id: diva2:1187200
Tillgänglig från: 2018-03-02 Skapad: 2018-03-02 Senast uppdaterad: 2018-03-02Bibliografiskt granskad

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