Serum homocysteine: Interplay with other circulating and genetic factors in association to Alzheimer's type dementia

Cascalheira, José F.; João, Sara S.; Pinhanços, Sandra S.; Castro, Rita; Palmeira, Manuela; Almeida, Sofia; Faria, Maria C.; Domingues, Fernanda

doi:10.1016/j.clinbiochem.2009.02.006

Cited by 30 publications

(32 citation statements)

References 37 publications

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“…[11][12][13] Accordingly, in the present study, a higher serum concentration of homocysteine, a lower concentration of vitamin B 12 and the MTHFR 1298A!C genetic polymorphism were associated with ATD, supporting previous findings. 3,11,13 Association of the TCN2 776C!G genetic polymorphism with ATD Variants of TC might potentially influence cellular availability of vitamin B 12 15,17,18 and thus contribute to the association between disrupted one-carbon metabolism and ATD. Therefore, the association of the TCN2 776C!G polymorphism with ATD, together with other factors involved in one-carbon metabolism, was addressed in the present study.…”

Section: Altered One-carbon Metabolism In Atdmentioning

confidence: 99%

Association of the transcobalamin II gene 776C→G polymorphism with Alzheimer’s type dementia: dependence on the 5, 10-methylenetetrahydrofolate reductase 1298A→C polymorphism genotype

et al. 2014

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Section: Altered One-carbon Metabolism In Atdmentioning

confidence: 99%

Association of the transcobalamin II gene 776C→G polymorphism with Alzheimer’s type dementia: dependence on the 5, 10-methylenetetrahydrofolate reductase 1298A→C polymorphism genotype

et al. 2014

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“…4, is arguably the most studied gene in this pathway, with 5,032 hits when queried on GOPUBMED (http://gopubmed.org, accessed 5-21-2013). Variations in this gene are associated with many disorders, including vascular disease, Alzheimer disease, neural tube defects, and cancer (Cascalheira et al 2009;Haviv et al 2002;Matakidou et al 2007;Shields et al 1999). MTHFR is responsible for conversion of 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate with a riboflavin cofactor (Ward et al 2011).…”

Section: Utilizes Gene Products Frommentioning

confidence: 99%

“…The 677C[T mutation reduces the effectiveness of MTHFR's enzyme activity, leading to increased homocysteine compared with the wild-type (C) allele (Yang et al 2008). Dysregulated homocysteine levels are linked to multiple diseases, many of which are exacerbated when coupled with low vitamin levels (Cascalheira et al 2009;Kelemen et al 2008;Zittan et al 2007). …”

Section: Utilizes Gene Products Frommentioning

confidence: 99%

“…Independent studies have already documented evidence that optimal vitamin intakes within a population vary due to single-nucleotide differences in genes within the OCM pathway (Bailey and Gregory 1999;Kelemen et al 2008;Stover and Garza 2002;Yang et al 2008;Zittan et al 2007). In addition to altered vitamin requirements, individuals with SNPs in genes encoding for enzymes residing along this pathway may also have increased susceptibility for comorbidity risk factors such as hyperhomocysteinemia (Garrod et al 2010) and diseases such as Alzheimer's type dementia (Cascalheira et al 2009) and cancer (Matakidou et al 2007;Vlastos et al 2009). …”

Section: Introductionmentioning

confidence: 99%

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Concept mapping One-Carbon Metabolism to model future ontologies for nutrient–gene–phenotype interactions

et al. 2014

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Advances in the development of bioinformatic tools continue to improve investigators' ability to interrogate, organize, and derive knowledge from large amounts of heterogeneous information. These tools often require advanced technical skills not possessed by life scientists. User-friendly, low-barrier-to-entry methods of visualizing nutrigenomics information are yet to be developed. We utilized concept mapping software from the Institute for Human and Machine Cognition to create a conceptual model of diet and health-related data that provides a foundation for future nutrigenomics ontologies describing published nutrient-gene/polymorphism-phenotype data. In this model, maps containing phenotype, nutrient, gene product, and genetic polymorphism interactions are visualized as triples of two concepts linked together by a linking phrase. These triples, or ''knowledge propositions,'' contextualize aggregated data and information into easy-to-read knowledge maps. Maps of these triples enable visualization of genes spanning the One-Carbon Metabolism (OCM) pathway, their sequence variants, and multiple literature-mined associations including concepts relevant to nutrition, phenotypes, and health. The concept map development process documents the incongruity of information derived from pathway databases versus literature resources. This conceptual model highlights the importance of incorporating information about genes in upstream pathways that provide substrates, as well as downstream pathways that utilize products of the pathway under investigation, in this case OCM. Other genes and their polymorphisms, such as TCN2 and FUT2, although not directly involved in OCM, potentially alter OCM pathway functionality. These upstream gene products regulate substrates such as B12. Constellations of polymorphisms affecting the functionality of genes along OCM, together with substrate and cofactor availability, may impact resultant phenotypes. These conceptual maps provide a foundational framework for development of nutrient-gene/polymorphism-phenotype ontologies and systems visualization.

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“…Uric acid (UA) is a particularly interesting molecule that may be involved in the pathogenesis of AD, HD, PD, and MS [1–4]. AD is the most common cause of dementia affecting estimated 24 million people worldwide [5] due to loss of neurons and synapses in the cerebral cortical and certain subcortical regions.…”

Section: Introductionmentioning

confidence: 99%

A Double-edged Sword: Uric Acid and Neurological Disorders

Luo

et al. 2013

Brain Disord Ther

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Uric Acid (UA), historically considered as a waste of cellular metabolism, has now received increasing attention because it was found to directly participate in the pathogenesis of many human diseases including neurological disorders. On one hand, low levels of UA are detrimental to the neurons because of its induction it impairs antioxidant capacity in the cell. High levels of UA, on the other hand, lead to an inflammatory response contributing to gout or neuroprotection. In this review, we summarize this biphasic function of uric acid and highlight potential therapeutic targets to treat UA-related neurological diseases.

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Serum homocysteine: Interplay with other circulating and genetic factors in association to Alzheimer's type dementia

Cited by 30 publications

References 37 publications

Association of the transcobalamin II gene 776C→G polymorphism with Alzheimer’s type dementia: dependence on the 5, 10-methylenetetrahydrofolate reductase 1298A→C polymorphism genotype

Association of the transcobalamin II gene 776C→G polymorphism with Alzheimer’s type dementia: dependence on the 5, 10-methylenetetrahydrofolate reductase 1298A→C polymorphism genotype

Concept mapping One-Carbon Metabolism to model future ontologies for nutrient–gene–phenotype interactions

A Double-edged Sword: Uric Acid and Neurological Disorders

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