ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Normalization of hyperhomocysteinemia improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer's disease.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Maternal hyperhomocysteinemia compromises female offspring fertility through overactivation of primordial follicles.iScience · 2026Article
- Hyperhomocysteinemia and Disease-Is 10 μmol/L a Suitable New Threshold Limit?International journal of molecular sciences · 2024Review
- Blood and CSF Homocysteine Levels in Alzheimer's Disease: A Meta-Analysis and Meta-Regression of Case-Control Studies.Neuropsychiatric disease and treatment · 2022Review
- Hyperhomocysteinemia: Metabolic Role and Animal Studies with a Focus on Cognitive Performance and Decline-A Review.Biomolecules · 2021Review
- Deciphering the Link Between Hyperhomocysteinemia and Ceramide Metabolism in Alzheimer-Type Neurodegeneration.Frontiers in neurology · 2019Article
- Genetic absence of ALOX5 protects from homocysteine-induced memory impairment, tau phosphorylation and synaptic pathology.Human molecular genetics · 2017Article
- Five lipoxygenase hypomethylation mediates the homocysteine effect on Alzheimer's phenotype.Scientific reports · 2017Article
- Serum Homocysteine, Dehydroepiandrosterone Sulphate and Lipoprotein (a) in Alzheimer's Disease and Vascular Dementia.Aging and disease · 2013Article
- Homocysteine imbalance: a pathological metabolic marker.Advances in nutrition (Bethesda, Md.) · 2012Review
- 5-Lipoxygenase gene transfer worsens memory, amyloid, and tau brain pathologies in a mouse model of Alzheimer disease.Annals of neurology · 2012Article
- Adeno-associated virus-mediated brain delivery of 5-lipoxygenase modulates the AD-like phenotype of APP mice.Molecular neurodegeneration · 2012Article
- Transcriptional regulation of β-secretase-1 by 12/15-lipoxygenase results in enhanced amyloidogenesis and cognitive impairments.Annals of neurology · 2012Article
- Is hyperhomocysteinemia an Alzheimer's disease (AD) risk factor, an AD marker, or neither?Trends in pharmacological sciences · 2011Review
- Homocysteine-mediated modulation of mitochondrial dynamics in retinal ganglion cells.Investigative ophthalmology & visual science · 2011Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Hyperhomocysteine (HHcy) is a risk factor for developing Alzheimer's disease (AD). Previously, we showed that diet-induced HHcy accelerated the AD-like phenotype of a transgenic mouse model, i.e., Tg2576. In the present work, we tested whether an HHcy-lowering strategy in this model would be beneficial. Tg2576 mice received methionine-rich or regular chow diet for 5 mo. Next, while the chow control group was kept on the same regimen, the other mice were randomized into two groups: one was kept on the methionine-rich diet (Met On), the other switched to chow (Met Off). Compared with controls, 5 mo on the methionine-rich diet resulted in HHcy (plasma Hcy level, treated: 12.7±1.2 μM vs. control: 3.1±0.4 μM) and significant behavioral impairments (% freezing, treated: 2.4±1.4% vs. control: 19.9±6.9%). At the end of the study, while the Met On group kept Hcy level elevated, the Met Off group had these values indistinguishable from the controls. The reduction in Hcy levels resulted in a significant improvement of the fear-conditioning performance, and an amelioration of the brain amyloidosis. Our results demonstrate that lowering HHcy in a transgenic AD-mouse model is beneficial since it significantly improves behavior deficits and brain amyloidosis. Our findings provide new biological insights for future clinical trials aimed at lowering this modifiable risk factor in human AD.
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