HIGHLIGHTS
SUMMARY
The disruption of ER homeostasis can lead to ER stress under persistent stress insult, which evidenced by the alternations in cellular Ca+ concentration and the over-accumulation of unfolded or misfolded proteins (Adamopoulos et_al, 2014; Leprivier et_al, 2015), eventually resulting in various protein-folding diseases, including AD (Salminen et_al, 2009; Li et_al, 2015). Other studies proved that ER stress-induced CHOP activation may participate in triggering AD-like pathology via promoting oxidative damage and reinforcing Abeta production (McCullough et_al, 2001; Ghribi et_al, 2006). (Lee, 2005; Yang et_al, 2013; Yatchenko et_al, 2019). AD patients presented . . .
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