荷兰神经科学研究所的研究人员在《Cell Stem Cell》期刊发表最新成果，揭示了部分高龄人群虽存在阿尔茨海默病脑部病理改变却未发展出痴呆症状的潜在生物学机制 1。据研究人员Evgenia Salta介绍，约30%出现相关脑部变化的老年人始终保持着认知健康，这一现象被称为“认知韧性” 1。为了探究其成因，研究团队对比了三组不同状态的人群：无病理改变者、已发展为痴呆的患者以及拥有病理特征但认知功能保持健康的个体 1。
研究发现，即使在遭受病理影响的大脑中，未成熟神经元依然存在；但在认知健康的群体体内，这些细胞并非仅仅通过数量增加来替换受损组织，而是激活了特定的生存和保护程序以对抗炎症与细胞死亡 1。具体而言，具备认知韧性的个体中，未成熟神经元表现出更强的抗损伤生物过程活性，同时伴随较低的炎症和细胞死亡信号 1。研究人员提出假设，认为这些细胞可能像“花园中的肥料”一样发挥支持作用，协助维持周围组织的健康，而不仅仅是直接替代死亡的神经元 1。尽管该发现为理解认知韧性提供了新线索，并可能引导未来治疗策略从修复损伤转向保护大脑功能，但目前结论主要基于脑组织观察数据，尚未通过实验直接证实这些细胞的具体功能 1。
Researchers at the Netherlands Institute for Neuroscience have identified a potential biological mechanism explaining why some individuals maintain cognitive health despite exhibiting brain pathology associated with Alzheimer’s disease 1. According to Evgenia Salta, approximately 30% of elderly people who display Alzheimer’s-related changes in their brains never develop dementia symptoms 1. The study, published in Cell Stem Cell on October 27, 2026, compared three distinct groups: those without pathological changes, patients who progressed to dementia, and individuals with pathology but preserved cognitive function 1.
The findings suggest that immature neurons play a critical role in "cognitive resilience" not by increasing in number to replace damaged cells, but by activating survival and protective programs 1. In cognitively healthy individuals with pathology, these immature neurons exhibited stronger activation of biological processes related to survival and resistance to damage, alongside lower signals of inflammation and cell death compared to those who developed dementia 1. The researchers hypothesize that these cells may support surrounding tissue, functioning like "fertilizer in a garden," rather than simply acting as substitutes for dying neurons 1. However, the authors note that this conclusion is based on observational data from brain tissue and has not yet been directly confirmed through experimental verification of specific cellular functions 1.
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