Walker Lary C, Jucker Mathias
Department of Neurology and Yerkes National Primate Research Center, Emory University, Atlanta, GA 30322, USA.
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, and the German Center for Neurodegenerative Diseases (DZNE), D-72076 Tübingen, Germany.
Trends Mol Med. 2017 Jun;23(6):534-545. doi: 10.1016/j.molmed.2017.04.001. Epub 2017 May 5.
Like many humans, non-human primates deposit copious misfolded Aβ protein in the brain as they age. Nevertheless, the complete behavioral and pathologic phenotype of Alzheimer's disease, including Aβ plaques, neurofibrillary (tau) tangles, and dementia, has not yet been identified in a non-human species. Recent research suggests that the crucial link between Aβ aggregation and tauopathy is somehow disengaged in aged monkeys. Understanding why Alzheimer's disease fails to develop in species that are biologically proximal to humans could disclose new therapeutic targets in the chain of events leading to neurodegeneration and dementia.
与许多人类一样，非人灵长类动物随着年龄增长会在大脑中沉积大量错误折叠的Aβ蛋白。然而，在非人类物种中尚未发现阿尔茨海默病完整的行为和病理表型，包括Aβ斑块、神经原纤维（tau）缠结和痴呆。最近的研究表明，在老年猴子中，Aβ聚集与tau病变之间的关键联系在某种程度上被打破了。了解为什么在与人类生物学关系密切的物种中不会发生阿尔茨海默病，可能会揭示导致神经退行性变和痴呆的一系列事件中的新治疗靶点。
