A hypothesis that proposes that in ALDH18A1 spastic paraplegia, the failure to produce specific proline residues required for the binding of SEC23IP as part of the COP2 transport process could be causative of symptoms and may be a viable treatment target

A hypothesis that proposes that in ALDH18A1 spastic paraplegia, the failure to produce specific proline residues required for the binding of SEC23IP as part of the COP2 transport process could be causative of symptoms and may be a viable treatment target

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