BAP31 deficiency contributes to the formation of amyloid‐β plaques in Alzheimer's disease by reducing the stability of RTN3

• DOI: 10.1096/fj.201801702r
• Publication Date: 2018-12-31T19:41:26Z
• Authors: Tianyi Wang; Jing Chen; Yue Hou; Yang Yu; Bing Wang
• Keywords: BACE1-AS; Amyloid (mycology); P3 peptide

Reticulon (RTN) 3 reduces amyloid-β (Aβ) plaques (APs) by negative modulation of β-secretase 1 (BACE1) activity. However, RTN3 aggregates easily, which offsets RTN3's inhibitory effect on BACE1 activity and exacerbates AP deposition. We found that BAP31 was a binding partner positively correlated with the expression level RTN3. To further explore how is involved in Alzheimer's disease (AD), conditional knockout mice targeted deletion (B-KO) hippocampus cerebral cortex were generated hybridized amyloid precursor protein (APP) PS1 transgenic (AD model) to obtain B-KO-AD mice. knock out primary hippocampal neurons decreased monomer availability enhanced aggregates, indicating deficiency increases instability More importantly, these effects contributed BACE1-mediated APP processing responsible for increased APs Thus, elevated human brain likely reduce formation both Aβ enhancing stability RTN3.—Wang, T., Chen, J., Hou, Y., Yu, Wang, B. contributes reducing FASEB J. 33, 4936–4946 (2019). www.fasebj.org