数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
Patients with Alzheimer’s disease (AD) suffer from progressively worsening dementia as the core clinical manifestation, accompanied by impaired quality of life and substantial family caregiver burden, all of which urgently need to be addressed.
方法
In this review, we propose the iron–mitochondria–oligodendrocyte axis (IMOA) as a new conceptual framework.
核心结论
Pathophysiologically, AD was traditionally defined as a continuum of neurodegenerative processes driven by the accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles (NFTs), independent of clinical symptoms.；Reciprocal Amplification with Amyloid-β and Tau Pathologies Rather than acting as an isolated pathway, OL ferroptosis engages in a reciprocal amplification loop with canonical AD pathologies.；Pharmacological modulation of the wingless/integrated-β-catenin (Wnt/β-catenin) and mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK/MAPK) signaling pathways, as well as treatment with celastrol, has been shown to overcome the differentiation block and enhance remyelination in the iron-overloaded AD brain [32,63,64,114]. ‖ 结论：Ultimately, IMOA can help us break free from the limitations of the amyloid-β and Tau hypotheses, and it will pave the way for innovative, multi-target diagnostic and therapeutic architectures that address the complex biological reality of AD.
局限
全文未设独立 limitations 节；结构上为综述/二次研究，因果推断强度受限。
对本项目的价值
★★★★☆ 脑老化是最大未满足需求，也是终点最难量化的领域；biomarker 与认知读数选择最敏感。命中核心 线粒体；设计 多组学。
全文来源
PMC JATS 全文（正文 25,998 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：The Iron-Mitochondria-Oligodendrocyte Axis: An Emerging Metabolic Framework for Alzheimer's Disease.
- 期刊与标识：Brain Sci · PMID 42939350 · DOI 10.3390/brainsci16101097**
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