“…The treatment, however, did not cause formation of CTD fragments, ubiquitination or phosphorylation of TDP-43 (Caragounis et al, 2010). Although an indirect route was not ruled out, especially via the generation of ROS through NMDA-or mitochondrial-mediated pathways by Zn 2+ , zinc ions are also known to bind and promote in vitro aggregation of Tau (Huang et al, 2014), alpha-synuclein (αSyn) (Valiente-Gabioud et al, 2012) and Amyloid-β Peptide(Aβ) (Alies et al, 2016). Altered zinc homeostasis is also suggested as a risk factor for several neurodegenerative disorders such as ALS or Alzheimer's disease [see review (Szewczyk, 2013)].…”