CBS and Alzheimer disease: While Sestrin2 protein levels were largely unaltered in Cbs-deficient mice (a mouse model showing chronically high Hcy levels as well as a subset of AD hallmarks), it is likely that deficiency in Sestrin2 is implicated in very early events of AD pathology, rendering cells insensitive to amino acid starvation and unable to reduce activity of their mTORC1 [5].