时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
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摘要（PubMed 原文节选）
Alzheimer's disease (AD) is a progressive neurodegenerative condition characterised by gradual neuronal degradation, resulting in cognitive decline and memory loss. Multiple pathogenic mechanisms drive the progression of the disease, including amyloid-β (Aβ) and tau accumulation (neurofibrillary tangles), mitochondrial dysfunction, synaptic loss, chronic neuroinflammation, and neuronal death. Neuronal loss in AD occurs through various forms of regulated cell death, including apoptosis, ferroptosis, pyroptosis, parthanatos, and necroptosis, each characterised by specific pathways and subsequent inflammatory consequences. Despite decades of focus on apoptosis and necrosis as the primary modes…
对本项目的价值
参考价值：属「线粒体质量控制与氧化应激」方向；脑老化 / 神经退行 / 认知栏目可用作本项目文献库与综述素材。 ｜ 价值分 1.5/5（★★☆☆☆）
全文不可及原因
无 PMCID 且 OpenAlex / Unpaywall 未提供可下载 OA PDF
原文题录
- 中文题名：靶向 RIPK1-NF-κB 交互：阿尔茨海默病坏死性凋亡的新视角
- 英文标题：Targeting RIPK1-NF-κB crosstalk: A novel perspective on necroptosis in Alzheimer's Disease.
- 期刊与标识：Mol Biol Rep · PMID 42967243 · DOI 10.1007/s11033-026-13067-0 · EDAT 2026-11-01