INT282439
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In addition, it is still unknown whether alterations in AdoMet and AdoHcy levels are cause or consequence of AD pathology. | |||||||||||||||
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In addition, we showed that cholesterol-containing, or DHA-enriched diets did not affect AdoMet or AdoHcy levels in brain tissue of APP/PS1 and wild-type mice. | |||||||||||||||
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If the above-mentioned hypothesis is valid, and AdoMet remains unaltered in aged APP/PS1 mice compared to young APP/PS1 mice, because of less demand for methylation due to neurodegeneration, AdoHcy levels will also be expected to be decreased or unchanged. | |||||||||||||||
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The finding that cholesterol- or DHA-containing diets do not alter AdoMet or AdoHcy levels in brain tissue of either wild type or APP/PS1 mice, but in contrast do have effects on AD pathology and cerebral hemodynamics [7, 15, 29], suggests that cholesterol- or DHA-containing diets do not influence cerebral hemodynamics or AD pathology via the methylation cycle. | |||||||||||||||
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Neither a cholesterol- nor a DHA-containing diet did alter AdoMet or AdoHcy levels in brain tissue of 8- and 15-month-old APP/PS1 and wild-type mice as compared to the standard diet (data not shown).
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The finding that AdoMet levels significantly differ only in 15-month-old APP/PS1 mice compared to their wild-type littermates, but not in 8-month-old mice, also indicates that alterations in AdoMet levels are a consequence of AD pathology rather than a cause. | |||||||||||||||
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No changes in AdoMet and AdoHcy levels, and consequently in the ratio between AdoMet and AdoHcy levels (methylation index), were observed between 8-month-old wild type and APP/PS1 mice (Fig. 1ac). | |||||||||||||||
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AdoMet and AdoHcy might also influence AD like pathology and vascular health [16] and it could be hypothesized that the above-mentioned nutritional components may influence and AdoMet and AdoHcy levels as well.
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