In our study, the increased expression of Ttr in the hippocampus of the MRL/lpr lupus model, compared with both the MRL/+ and Fn14ko controls, may indicate a compensatory, protective mechanism that was driven in the lupus mice due to stress or local inflammation (there is no evidence in the literature for increased production of amyloid precursor proteins in the context of SLE, or NPSLE [66], and so it is unclear what is driving the increased expression of Ttr here). Here, TTR is linked to systemic lupus erythematosus.