Homocysteine, vitamin B6, and vascular disease in AD patients

J. W. Miller, Ralph Green, Dan M Mungas, Bruce R Reed, W. J. Jagust

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Abstract

Background: Cerebrovascular disease is a cause of dementia and is associated with elevated plasma levels of homocysteine. Patients with AD tend to have unexplained elevations of homocysteine concentrations vs healthy control subjects. Vitamin B6 status, a potential determinant of plasma homocysteine, has not been characterized in patients with AD. Objective: To investigate plasma homocysteine, vitamin B6 status, and the occurrence of vascular disease in patients with AD. Methods: Forty-three patients with AD and 37 control subjects without AD were studied for homocysteine, B vitamin status (folate, vitamin B12 pyridoxal-5′- phosphate [PLP]), kidney function (creatinine), and thyroid function (thyroid-stimulating hormone, thyroxin). In addition, the presence of vascular disease was assessed by reviewing both medical histories and brain imaging data provided by CT and MRI. Results: The OR for elevated plasma homocysteine (>12 μmol/L) was only 2.2 (not significant) for subjects with AD. In contrast, the OR was 10.0 (p = 0.03) for subjects with vascular disease (n = 26). The OR for low plasma PLP (< 25 nmol/L) was 12.3 (p = 0.01) for patients with AD. No significant relationship was observed between vascular disease and PLP level or between plasma homocysteine and PLP concentrations. Conclusions: Elevated plasma homocysteine in patients with AD appears related to vascular disease and not AD pathology. In addition, low vitamin B6 status is prevalent in patients with AD. It remains to be determined if elevated plasma homocysteine or low vitamin B6 status directly influences AD pathogenesis or progression.

Original languageEnglish (US)
Pages (from-to)1471-1475
Number of pages5
JournalNeurology
Volume58
Issue number10
StatePublished - May 28 2002

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ASJC Scopus subject areas

  • Neuroscience(all)

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