Autophagy-lysosome dysfunction is involved in Aβ deposition in STZ-induced diabetic rats

•In this research, these findings indicated that diabetes activated autophagy, but lysosome function was impaired.•Autophagy-lysosome dysfunction may be involved in the Aβ deposition in diabetic cognitive impairment.•As the time advanced, the Aβ deposition was getting worse in hippocampus of diabeti...

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Veröffentlicht in:Behavioural brain research 2017-03, Vol.320, p.484-493
Hauptverfasser: Ma, Lou-Yan, Lv, Ya-Li, Huo, Kang, Liu, Jie, Shang, Su-Hang, Fei, Yu-Lang, Li, Yan-Bo, Zhao, Bei-Yu, Wei, Meng, Deng, Yong-Ning, Qu, Qiu-Min
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Sprache:eng
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Zusammenfassung:•In this research, these findings indicated that diabetes activated autophagy, but lysosome function was impaired.•Autophagy-lysosome dysfunction may be involved in the Aβ deposition in diabetic cognitive impairment.•As the time advanced, the Aβ deposition was getting worse in hippocampus of diabetic rats. β-Amyloid (Aβ) deposition has a central role in the pathogenesis of Alzheimer disease (AD). Previous studies have indicated that as a risk factor for AD, diabetes mellitus (DM) could induce Aβ deposition in the brain, but the mechanism is not fully elucidated. Autophagy-lysosome is a cellular pathway involved in protein and organelle degradation. In the present study, we used streptozotocin (STZ)-induced diabetic rats to investigate whether autophagy-lysosome is related to Aβ1-42 clearance in DM. We found that DM rats had a longer escape latency and less frequent entry into the target zone than that of the control group (p
ISSN:0166-4328
1872-7549
DOI:10.1016/j.bbr.2016.10.031