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.

中文翻译：

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人类对阿尔茨海默氏病的特殊脆弱性

像许多人类一样，非人类的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。尽管如此，尚未在非人类物种中发现阿尔茨海默氏病的完整行为和病理表型，包括Aβ斑块，神经原纤维缠结和痴呆。最近的研究表明，在老龄猴子中，Aβ聚集与tauopathy之间的关键联系已经脱离。了解为什么阿尔茨海默氏症无法在生物学上接近人类的物种中发展，可能会在导致神经变性和痴呆的一系列事件中揭示新的治疗靶标。