These findings directly link Hcy-thiolactone and N-Hcy-protein with dysregulated mTOR signaling (Fig. 3C, D) and its downstream outcomes such as impaired autophagy flux (Fig. 3I, J, K, L) and increased Aβ accumulation (Fig. 5) thereby providing a likely mechanism explaining neuropathy resulting from Blmh deficiency (Fig. 7) and accounting for the association of HHcy with AD [53]. This evidence concerns the gene BLMH and Alzheimer disease.