Is aberrant localization of FUS and TDP43 associated with misfolding of SOD1 in amyotrophic lateral sclerosis?
We conclude that cytosolic mislocalization of FUS or TDP43 in vitro and ALS in vivo may kindle wtSOD1 misfolding in non-SOD1 FALS and SALS. The lack of immunohistochemical compartmental co-localization of misfolded SOD1 with cytosolic TDP43 or FUS suggests an indirect induction of SOD1 misfolding followed by propagation through template directed misfolding beyond its site of inception. The identification of a final common pathway in the molecular pathogenesis of ALS provides a treatment target for this devastating disease.
The preoperative Lee Risk Index is not only an important prognostic factor for in-hospital outcome but also for late mortality and impaired health status in patients with peripheral arterial disease.