Brain ATP:l-methionine S-adenosyltransferase (MAT), S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH): regional distribution and age-related changes

Trolin, Cecilia Gomes; Löfberg, Charlotta; Trolin, G.; Oreland, Lars

doi:10.1016/0924-977x(94)90295-x

Cited by 28 publications

(7 citation statements)

References 51 publications

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“…In this regard, SAM levels and activity of the enzyme responsible for its generation (methionine‐S‐adenosyltransferase) were decreased in brain tissue of individuals exhibiting neurodegeneration (Bottiglieri et al. 1990; Trolin et al. 1994; Morrison et al.…”

Section: Discussionmentioning

confidence: 99%

Dietary deficiency increases presenilin expression, gamma‐secretase activity, and Abeta levels: potentiation by ApoE genotype and alleviation by S‐adenosyl methionine

Chan

Tchantchou

Rogers

et al. 2009

Journal of Neurochemistry

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Apolipoprotein E4 (ApoE4) is a risk factor for Alzheimer’s disease (AD). Whether this risk arises from a deficient function of E4 or the lack of protection provided by E2 ir E3 is unclear. Previous studies demonstrate that deprivation of folate and vitamin E, coupled with dietary iron as a pro‐oxidant, for 1 month displayed increased presenilin 1 (PS‐1) expression, gamma‐secretase, and Abeta generation in mice lacking ApoE (ApoE−/− mice). While ApoE−/− mice are a model for ApoE deficiency, they may not reflect the entire range of consequences of E4 expression. We therefore compared herein the impact of the above deficient diet on mice expressing human E2, E3, or E4. As folate deficiency is accompanied by a decrease in the major methyl donor, S‐adenosyl methionine (SAM), additional mice received the deficient diet plus SAM. E2 was more protective than murine ApoE or E3 and E4. Surprisingly, PS‐1 and gamma‐secretase were over‐expressed in E3 to the same extent as in E4 even under a complete diet, and were not alleviated by SAM supplementation. Abeta increased only in E4 mice maintained under the complete diet, and was alleviated by SAM supplementation. These findings suggest dietary compromise can potentiate latent risk factors for AD.

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Section: Discussionmentioning

confidence: 99%

Dietary deficiency increases presenilin expression, gamma‐secretase activity, and Abeta levels: potentiation by ApoE genotype and alleviation by S‐adenosyl methionine

Chan

Tchantchou

Rogers

et al. 2009

Journal of Neurochemistry

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“…Expression of DNMT3B decreases with age in at least some tissues, perhaps promoting age-associated hypomethylation of some clock CpGs (Armstrong et al, 2014; Ciccarone et al, 2016). Levels of SAM have been reported to decrease with age (Geller et al, 1988; Hoffman et al, 1979; Stramentinoli et al, 1977; Trolin et al, 1994). Mitochondrial function, important for production of α-KG, also declines with age (Sun et al, 2016).…”

Section: What Is the Mechanism Underlying The Clocks?mentioning

confidence: 99%

DNA Methylation Clocks in Aging: Categories, Causes, and Consequences

et al. 2018

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Age-associated changes to the mammalian DNA methylome are well documented and thought to promote diseases of aging, such as cancer. Recent studies have identified collections of individual methylation sites whose aggregate methylation status measures chronological age, referred to as the DNA methylation clock. DNA methylation may also have value as a biomarker of healthy versus unhealthy aging and disease risk; in other words, a biological clock. Here we consider the relationship between the chronological and biological clocks, their underlying mechanisms, potential consequences, and their utility as biomarkers and as targets for intervention to promote healthy aging and longevity.

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“…With age, the activities of methionine adenosyltransferase, betaine homocysteine methyltransferase and methionine synthase decrease while cystathionine synthase and cystathionase increase (Finkelstein et al 1971). Moreover, the concentration of AdoMet decrease and that of AdoHcy increases in liver and brain (Trolin et al 1994;Varela-Moreiras et al 1994). The changes in methionine metabolism influence the aging process through protein and DNA methylation (Chiang et al 1996) and glutathionemediated antioxidative defense mechanism (Wu et al 2004).…”

Section: Discussionmentioning

confidence: 92%

Continuous oxidative stress due to activation of polyamine catabolism accelerates aging and protects against hepatotoxic insults

et al. 2010

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Enhanced polyamine catabolism via polyamine acetylation-oxidation elevates the oxidative stress in an organism due to increased production of reactive oxygen species (ROS). We studied a transgenic mouse line overexpressing the rate limiting enzyme in the polyamine catabolism, spermidine/spermine N (1)-acetyltransferase (SSAT) that is characterized by increased putrescine and decreased spermidine and spermine pools. In order to protect the mice from the chronic oxidative stress produced by the activation of polyamine catabolism, the hepatic expression of the transcription factor p53 was found threefold elevated in the transgenic mice. In addition, the prolonged activation of p53 accelerated the aging of transgenic mice and reduced their lifespan (50%). Aging was associated with decreased antioxidant enzyme activities. In the transgenic mice the activities of catalase and Cu, Zn-superoxide dismutase (SOD) were 42 and 23% reduced respectively, while the expression of CYP450 2E1 was 60% decreased and oxidative stress measured as protein carbonyl content was tenfold elevated. In the transgenic mice, the age-related repression of the different antioxidant enzymes served as a protection against the hepatotoxic effects of carbon tetrachloride and thioacetamide.

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Brain ATP:l-methionine S-adenosyltransferase (MAT), S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH): regional distribution and age-related changes

Cited by 28 publications

References 51 publications

Dietary deficiency increases presenilin expression, gamma‐secretase activity, and Abeta levels: potentiation by ApoE genotype and alleviation by S‐adenosyl methionine

Dietary deficiency increases presenilin expression, gamma‐secretase activity, and Abeta levels: potentiation by ApoE genotype and alleviation by S‐adenosyl methionine

DNA Methylation Clocks in Aging: Categories, Causes, and Consequences

Continuous oxidative stress due to activation of polyamine catabolism accelerates aging and protects against hepatotoxic insults

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