| First Author | Xiao X | Year | 2019 |
| Journal | Neurobiol Aging | Volume | 81 |
| Pages | 77-87 | PubMed ID | 31252207 |
| Mgi Jnum | J:281641 | Mgi Id | MGI:6378394 |
| Doi | 10.1016/j.neurobiolaging.2019.05.016 | Citation | Xiao X, et al. (2019) ABAD/17beta-HSD10 reduction contributes to the protective mechanism of huperzine a on the cerebral mitochondrial function in APP/PS1 mice. Neurobiol Aging 81:77-87 |
| abstractText | Huperzine A (HupA) is a kind of Lycopodium alkaloid with potential disease-modifying qualities that has been reported to protect against beta-amyloid (Abeta)-mediated mitochondrial damage in Alzheimer's disease. However, the fundamental molecular mechanism underlying the protective action of HupA against Abeta-mediated mitochondrial malfunction is not completely understood. Recently, the mitochondrial enzyme amyloid-binding alcohol dehydrogenase (ABAD) protein has been reported to facilitate Abeta-induced mitochondrial damage, resulting in mitochondrial malfunction and cell death. Our study found that HupA, but not the acetylcholinesterase inhibitor tacrine, reduced the deposition of Abeta and the ABAD level, and further reduced Abeta-ABAD complexes, thereby improving cerebral mitochondrial function in APP/PS1 mice. This was accompanied by attenuated reactive oxygen species overload, as well as increases adenosine triphosphate levels. Moreover, HupA decreased the release of cytochrome-c from mitochondria and the level of cleaved caspase-3, thereby increasing dissociated brain cell viability in APP/PS1 mice. Thus, our study demonstrated that a reduction in ABAD was involved in the protective mechanism of HupA on the cerebral mitochondrial function in APP/PS1 mice. |
