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In reaction to AD, astrocytes experience a shift in profile, one that is reactive and pro-inflammatory while losing homeostatic roles thus disrupting BBB integrity, ion and neurotransmitter buffering, and energy metabolism (Liddelow et al., 2017
Based on basic MichaelisMenten enzyme kinetics, by supplying the extra substrate and cofactor (i.e., folate and riboflavin) the reduced affinity can be overcome and the consequences of having the variant can be alleviated, e.g., reduction in elevated homocysteine, reduction in blood pressure, etc. This is the very definition of personalized nutrition, in this case an increased requirement of two essential nutrients based on a common genetic difference
Some patients require a short course to correct deficiency, while others may benefit from maintenance injections over time
They're a very sharp blade and we want to use them potently
Hyperhomocysteinaemia and endothelial dysfunction in young patients with peripheral arterial occlusive disease
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