Editorial: Protein Misfolding and Spreading Pathology in Neurodegenerative Diseases

[...]TAR-DNA binding protein 43 (TDP-43)- or tau-positive inclusions can be found in the brain or spinal cord in, e.g., frontotemporal lobar degeneration (FTLD) or amyotrophic lateral sclerosis (ALS) (Arai et al., 2006; Hasegawa et al., 2008; Kabashi et al., 2008; Sreedharan et al., 2008; Da Cruz and Cleveland, 2011). Whether these clinical observations with Aβ and aSyn pathology represent authentic prion spreading of pathology remains controversial, and this issue calls for caution due to the tremendous implications it might have. [...]using prion-like terminology for all neurodegenerative diseases requires a deeper understanding of the molecular mechanisms involved. [...]Nam et al. discuss the efficacy of ALWPs, a combination of oriental herbal medicines with proven efficacy in diabetes mellitus, immune modulation, and owning both neurotrophic and anti-inflammatory action in decreasing Aβ plaque load, as well as Tau hyperphosphorylation in the cortex and hippocampus of the 5XFAD mouse model of AD. [...]the articles in this Research Topic provide new up-to-date insights into our understanding of protein aggregation and spreading of pathology in prion and prion-like neurodegenerative disorders.