<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cao, Shu-Qin</style></author><author><style face="normal" font="default" size="100%">Jiménez-Loygorri, Juan Ignacio</style></author><author><style face="normal" font="default" size="100%">Qiu, Yunguang</style></author><author><style face="normal" font="default" size="100%">Kang, You Jung</style></author><author><style face="normal" font="default" size="100%">Van Do, Khanh</style></author><author><style face="normal" font="default" size="100%">Smith, Annabel E</style></author><author><style face="normal" font="default" size="100%">Huang, Junjie</style></author><author><style face="normal" font="default" size="100%">Pan, Jun-Ping</style></author><author><style face="normal" font="default" size="100%">Mao, Lipeng</style></author><author><style face="normal" font="default" size="100%">Li, Ang</style></author><author><style face="normal" font="default" size="100%">Yang, Hangge</style></author><author><style face="normal" font="default" size="100%">Aman, Yahyah</style></author><author><style face="normal" font="default" size="100%">Lagartos, Maria Jose Donate</style></author><author><style face="normal" font="default" size="100%">Lautrup, Sofie Hindkjær</style></author><author><style face="normal" font="default" size="100%">Chen, Anbin</style></author><author><style face="normal" font="default" size="100%">Liang, Kristina Xiao</style></author><author><style face="normal" font="default" size="100%">Zhang, Hailong</style></author><author><style face="normal" font="default" size="100%">Yi, Juan</style></author><author><style face="normal" font="default" size="100%">Jin, Xurui</style></author><author><style face="normal" font="default" size="100%">Cheung, Tin Cho</style></author><author><style face="normal" font="default" size="100%">Apokotou, Olympia</style></author><author><style face="normal" font="default" size="100%">Papastefanaki, Florentia</style></author><author><style face="normal" font="default" size="100%">Matsas, Rebecca</style></author><author><style face="normal" font="default" size="100%">McEwan, William A</style></author><author><style face="normal" font="default" size="100%">Cheng, Feixiong</style></author><author><style face="normal" font="default" size="100%">Cho, Hansang</style></author><author><style face="normal" font="default" size="100%">Chen, Guobing</style></author><author><style face="normal" font="default" size="100%">Su, Huanxing</style></author><author><style face="normal" font="default" size="100%">Palikaras, Konstantinos</style></author><author><style face="normal" font="default" size="100%">Luo, Oscar Junhong</style></author><author><style face="normal" font="default" size="100%">Zhao, Qian Hua</style></author><author><style face="normal" font="default" size="100%">Ding, Ding</style></author><author><style face="normal" font="default" size="100%">van Duijn, Cornelia</style></author><author><style face="normal" font="default" size="100%">Tavernarakis, Nektarios</style></author><author><style face="normal" font="default" size="100%">Boya, Patricia</style></author><author><style face="normal" font="default" size="100%">Tencomnao, Tewin</style></author><author><style face="normal" font="default" size="100%">Fang, Evandro F</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The Mitochondrial Guardian α-Amyrin Mitigates Alzheimer's Disease Pathology via Modulation of the DLK-SARM1-ULK1 Axis</style></title><secondary-title><style face="normal" font="default" size="100%">Advanced science (Weinheim, Baden-Wurttemberg, Germany)</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Artificial Intelligence</style></keyword><keyword><style  face="normal" font="default" size="100%">cognitive function</style></keyword><keyword><style  face="normal" font="default" size="100%">dual leucine zipper kinase (DLK)</style></keyword><keyword><style  face="normal" font="default" size="100%">mitochondrial function</style></keyword><keyword><style  face="normal" font="default" size="100%">α‐Amyrin</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2026</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2026</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://dx.doi.org/10.1002/advs.202512374https://www.ncbi.nlm.nih.gov/pubmed/41572497https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13116123</style></url></web-urls></urls><pub-location><style face="normal" font="default" size="100%">Germany</style></pub-location><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">e12374</style></pages><isbn><style face="normal" font="default" size="100%">2198-3844</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">High consumption of colorful fruits and vegetables correlates with low dementia risk, but the exact molecules and the underlying biological mechanisms governing their bioactive profiles are largely unknown. Using a 10-year observational cohort study coupled with an AI-driven systems pharmacology platform, we identified a natural triterpenoid compound found in colorful fruits and vegetables, α-Amyrin (αA), as a therapeutic candidate for Alzheimer's disease (AD). The efficacy of αA in treating the symptoms of AD, such as Tau tangles, damaged mitochondria, and memory loss, was examined using cross-species models; αA retained memory in AD-like animal models while also strongly inhibiting Tau pathology, especially p-Tau217, in a cellular 'Tau seeding' system and in Tau[P301S] mice, followed by validation using a human 3D microfluidic system. At molecular level, αA is a robust mitochondrial regulator, enhancing mitochondrial stress resilience and activation of mitophagy. Mechanistically, αA inhibits dual leucine zipper kinase (DLK), leading to the inhibition of DLK-Sterile Alpha and TIR Motif Containing 1 (SARM1)-dependent neurodegeneration; this inhibition frees unc-51 Like Autophagy Activating Kinase 1 (ULK1) from the ULK1-SARM1 complex, allowing it to participate in autophagy/mitophagy. αA also shows strong translational potential with a 10.1 h half-life and the ability to cross the blood-brain barrier. Our results indicate that αA may act as a mitochondrial guardian against AD via modulating the DLK-SARM1-ULK1-autophagy/mitophagy axis while further preclinical and clinical studies are warranted.</style></abstract><issue><style face="normal" font="default" size="100%">24</style></issue></record></records></xml>