Journal
NEUROBIOLOGY OF AGING
Volume 28, Issue 8, Pages 1195-1205Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2006.05.035
Keywords
Alzheimer; amyloid; behavior; learning; water maze; memory; delayed non-matching to position; delayed conditional discrimination; transgenic; folate; folic acid; homocysteine
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Funding
- NIA NIH HHS [AG022439] Funding Source: Medline
- NICHD NIH HHS [HD015052] Funding Source: Medline
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Consumption of a diet that significantly elevates homocysteine (homocysteinemia) induces cell death in the CA3 hippocampal subfield in amyloid precursor protein (APP) over-expressing transgenic mice but not in wild-type controls. We assessed behavioral and other neuropathological effects of a homocysteinemia-inducing diet in aged APP-overexpres sing mice. Starting at 16-18 months of age, mice were fed either a treatment diet lacking folate, choline, and methionine, and supplemented with homocysteine, or a control diet containing normal amounts of folate, choline and methionine but no homocysteine. After 5 months on the experimental diets, performance on a delayed non-matching-to-position working-memory task was unimpaired. In contrast, spatial reference memory in the water maze was impaired in transgenic mice on the treatment diet. Transgenic mice had higher homocysteine levels than wild-type mice even when fed the control diet, suggesting an effect of genotype on homocysteine metabolism. Methyl-donor deficiency did not alter amyloid deposition in the transgenic mice. These results suggest that disrupted homocysteine metabolism may induce A beta-associated memory impairments and neurodegeneration in APP overexpressing truce. (c) 2006 Elsevier Inc. All rights reserved.
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