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Homocysteine concentrations in the cognitive progression of Alzheimer's disease.
Exp Gerontol. 2017 12 01; 99:146-150.EG

Abstract

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 13months. 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.

Authors+Show Affiliations

Centre for Dementia Studies, Brighton and Sussex Medical School, Brighton, BN1 9RY, UK. Electronic address: N.Farina@bsms.ac.uk.Department of Pharmacology, University of Oxford, Oxford OX1 3QT, UK.Department of Pharmacology, University of Oxford, Oxford OX1 3QT, UK.Department of Nutritional Sciences, University of Surrey, Guildford GU2 7XH, UK.Centre for Dementia Studies, Brighton and Sussex Medical School, Brighton, BN1 9RY, UK; Dementia Research Unit, Sussex Partnership NHS Foundation Trust, Crowborough TN6 1HB, UK.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29024723

Citation

Farina, Nicolas, et al. "Homocysteine Concentrations in the Cognitive Progression of Alzheimer's Disease." Experimental Gerontology, vol. 99, 2017, pp. 146-150.
Farina N, Jernerén F, Turner C, et al. Homocysteine concentrations in the cognitive progression of Alzheimer's disease. Exp Gerontol. 2017;99:146-150.
Farina, N., Jernerén, F., Turner, C., Hart, K., & Tabet, N. (2017). Homocysteine concentrations in the cognitive progression of Alzheimer's disease. Experimental Gerontology, 99, 146-150. https://doi.org/10.1016/j.exger.2017.10.008
Farina N, et al. Homocysteine Concentrations in the Cognitive Progression of Alzheimer's Disease. Exp Gerontol. 2017 12 1;99:146-150. PubMed PMID: 29024723.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Homocysteine concentrations in the cognitive progression of Alzheimer's disease. AU - Farina,Nicolas, AU - Jernerén,Fredrik, AU - Turner,Cheryl, AU - Hart,Kathryn, AU - Tabet,Naji, Y1 - 2017/10/10/ PY - 2017/05/11/received PY - 2017/10/04/revised PY - 2017/10/08/accepted PY - 2017/10/13/pubmed PY - 2018/6/26/medline PY - 2017/10/13/entrez KW - Alzheimer's disease KW - B vitamins KW - Cognition KW - Homocysteine SP - 146 EP - 150 JF - Experimental gerontology JO - Exp Gerontol VL - 99 N2 - 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 13months. 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. SN - 1873-6815 UR - https://www.unboundmedicine.com/medline/citation/29024723/Homocysteine_concentrations_in_the_cognitive_progression_of_Alzheimer's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0531-5565(17)30374-1 DB - PRIME DP - Unbound Medicine ER -