基础研究

臭氧作为 AD 与睡眠障碍的催化剂:空气污染假说被摆上桌面

来源:Biology (Basel) · PMID 42939505 · DOI 10.3390/biology15201904** · 来源:IMA 知识库《文献层·文献监控卡片》2026-10-29 期 · 全文级(file_id dGBunAeRiRlm,下载实测 692,872 B) · 全文已获取并通过归属校验

数据日期 2026-10-29 · 生成时间 2026-10-29 06:03

研究问题

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and hallmark neuropathological features, including β-amyloid (Aβ) plaque accumulation, hyperphosphorylated tau neurofibrillary tangles, oxidative stress, neuroinflammation, and synaptic dysfunction [1,2,3,4].

方法

(全文无独立方法节,正文亦未给出可抽取的实验动作句)

核心结论

Moreover, support for several steps (MAC1/NOX2, HMGB1/TREM2, lipid peroxidation by-products, gut–brain signaling) comes from non-ozone or indirect models (Section 2.2). ‖ 结论:We propose, as a working hypothesis, that these effects arise from a systemic oxidative–inflammatory signal that reaches the central nervous system, with sleep/circadian disruption and AD-related pathology as downstream outcomes that may reinforce each other.

局限

This discrepancy between a plausible mechanism and an inconsistent epidemiological signal may reflect several non-mutually exclusive factors: (i) exposure misclassification, since ambient ozone monitoring stations rarely capture individual indoor/outdoor exposure; (ii) confounding by co-pollutants, given that ozone rarely occurs in isolation from PM2.5 and NO2 in urban settings; (iii) differences in latency windows, as neurodegenerative outcomes may require decades of cumulative exposure while most cohorts have shorter follow-up; (iv) outcome heterogeneity, with some studies assessing clinical dementia and others subclinical biomarkers or sleep-specific endpoints; and (v) the possibility…

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;最大样本量约 395,651;设计 前瞻队列、观察性。

全文来源

PMC JATS 全文(正文 32,859 字符,已过标题/DOI 逐字归属校验)

原文题录

  • 英文标题:Ozone as a Catalyst for Alzheimer's Disease and Sleep Disorders: Implications for Neurodegeneration Induced by Air Pollution.
  • 期刊与标识:Biology (Basel) · PMID 42939505 · DOI 10.3390/biology15201904**

B 级证据分级:B 级(同行评议临床前研究,主要为动物模型)

本文核心结论来自动物模型或体外细胞学,属临床前证据,不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义,与人类临床结局之间仍有距离。

关于本文的文献来源:本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写,依据已获取的期刊全文(方法、样本量与结论已回到原文核对);未能获取全文的同批条目另行标注「摘要级」,全程未做任何数值推算补全。