时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
（原文未给出可直接抽取的对应表述）
方法
The following sections summarize key mechanisms of Aβ and tau in AD pathogenesis.2.1Aβ and Alzheimer’s diseaseAβ is the main component of extracellular amyloid plaques in the brain of patients with AD and has long been considered a key molecular driver of the occurrence and progression of the disease (Glenner and Wong, 1984).；Zhang et al. reported that in 13-month-old APP/PS1 mice, long-term autonomous wheel movement can improve learning and identification memory without affecting the exercise ability, reducing the Aβ plaque load of the hippocampal body, and increasing the volume of the dentate return and CA1 region.；In addition, Chen et al. found that in 6.5-month-old 5 × FAD mice, 1 month of treadmill training increased the tube diameter of the meningeal lymphatic vessels, enhanced its structural plasticity and drainage ability, and increased the transport of Aβ and glial fiber acid protein to deep cervical lymph nodes.
核心结论
In summary, exercise may delay the occurrence of AD and slow down the progression of the disease by accelerating the removal of Aβ.2.2Tau and ADUnder physiological conditions, tau protein is a microtubule-related protein in the neuronal cytoplasm, which is responsible for regulating microtubule dynamics and supporting axon transport and nerve process growth.；In summary, exercise training may effectively reduce pathological tau protein, thus delaying the onset of AD and slowing down the progression of the disease.3Neuroinflammation and ADIn addition to the Aβ and tau protein hypothesis, neuroinflammation also plays a crucial role in the occurrence and development of AD.；In human studies, although acute movement temporarily increases IL-6, it will then induce the production of anti-inflammatory mediators such as IL-1RA and IL-10, inhibit IL-1β signal conduction, and reduce inflammation-promoting factors such as TNF-α (Pinho et al., 2010).Overall, exercise may improve neuroinflammation in AD through four ways.
局限
However, in AD, tau protein will undergo abnormal phosphorylation, conformational changes, and wrong folding, leading to dissociation from microtubules and forming soluble oligomers and insoluble aggregates, and finally depositing to form NFTs (Iqbal et al., 2016).；However, more recent studies indicate that lactate in the brain can serve as an energy substrate (Brooks, 2020).；Nevertheless, several limitations and unresolved issues remain in current research.
对本项目的价值
中高价值：属「线粒体质量控制与氧化应激」方向；线粒体功能与氧化应激栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.4/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 35,188 字符，题名指纹 0.83，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：体育锻炼：阿尔茨海默病防治的多靶点策略
- 英文标题：Physical exercise: a multi-target strategy for the prevention and treatment of Alzheimer's disease.
- 期刊与标识：Frontiers in aging neuroscience · PMID 42973868 · DOI 10.3389/fnagi.2026.1876075 · PMC PMC13725395