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Homocysteine, vitamin B6, and vascular disease in AD patients
J W Miller1, R Green, D M Mungas
1Department of Medical Pathology, University of California, Davis, School of Medicine, Sacramento 95817, USA. jwmiller@ucdavis.edu
Insights
Elevated homocysteine in Alzheimer's disease (AD) is linked to vascular issues, not AD itself. Many AD patients show low vitamin B6 status, a finding needing further research into its role in AD progression.
Area of Science:
- Neurology
- Biochemistry
- Gerontology
Background:
- Cerebrovascular disease is a known cause of dementia.
- Elevated plasma homocysteine levels are associated with dementia and Alzheimer's disease (AD).
- Vitamin B6 status, a factor in homocysteine levels, has not been well-characterized in AD patients.
Purpose of the Study:
- To investigate plasma homocysteine and vitamin B6 status in AD patients.
- To determine the relationship between vitamin B6 status, homocysteine levels, and vascular disease in AD.
- To assess the prevalence of vascular disease in AD patients.
Main Methods:
- Studied 43 AD patients and 37 controls for homocysteine, B vitamin status (folate, B12, pyridoxal-5'-phosphate [PLP]), kidney, and thyroid function.
- Assessed vascular disease presence using medical histories and brain imaging (CT, MRI).
Main Results:
- Elevated plasma homocysteine was not significantly associated with AD but strongly linked to vascular disease (OR=10.0, p=0.03).
- Low plasma PLP (<25 nmol/L) was prevalent in AD patients (OR=12.3, p=0.01).
- No significant correlation found between vascular disease and PLP, or between plasma homocysteine and PLP.
Conclusions:
- Elevated homocysteine in AD patients is likely due to co-existing vascular disease, not AD pathology.
- Low vitamin B6 status is common in individuals with AD.
- Further research is needed to clarify if homocysteine or vitamin B6 status directly impacts AD pathogenesis or progression.
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 B(6) status, a potential determinant of plasma homocysteine, has not been characterized in patients with AD.
Objective:
To investigate plasma homocysteine, vitamin B(6) 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 B(12), 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 micromol/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 B(6) status is prevalent in patients with AD. It remains to be determined if elevated plasma homocysteine or low vitamin B(6) status directly influences AD pathogenesis or progression.