代谢组学
生物
神经科学
代谢组
海马结构
代谢途径
认知功能衰退
糖酵解
转录组
代谢物
疾病
质谱成像
胆碱能的
海马体
代谢网络
阿尔茨海默病
锡尔图因
生物信息学
计算生物学
SIRT2
脂质代谢
鞘脂
神经保护
脂类学
厌氧糖酵解
机制(生物学)
串联质量标签
信号转导
痴呆
缺血
作者
Lin Liu,Yang Yang,Ze-Jie Qu,Shuang Wu,Xiang Zou,Dongxue Wang
标识
DOI:10.1021/acschemneuro.5c00528
摘要
Vascular cognitive impairment (VCI) significantly contributes to dementia; however, the precise metabolic mechanisms underlying its region-specific pathological progression remain poorly understood. We hypothesized that spatially resolved metabolomics could uncover detailed spatiotemporal metabolic disruptions and key therapeutic windows. Using matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI), we systematically mapped metabolite alterations in hippocampal subregions (CA1, CA3, dentate gyrus) and cortical areas of a rat model of chronic cerebral hypoperfusion (2-VO) at early (7 days), intermediate (28 days), and late (56 days) stages. MALDI-MSI enabled region-resolved visualization of lipid, energy, and inflammatory metabolic signatures at a spatial resolution of 20 μm, allowing comparative analysis of spatiotemporal metabolic trajectories across disease progression. Our analysis revealed distinct temporal patterns: early depletion of membrane lipids and cholinergic precursors primarily in CA1 and DG, midphase ceramide accumulation and glycolytic shift notably in CA3 at day 28, and widespread mitochondrial dysfunction with necroptotic signaling by day 56. Critical metabolic putative markers─including PC(15:0/16:0), CerP(d18:1/18:0), and LysoPA(0:0/18:1)─delineated disease stages, establishing day 28 as a pivotal therapeutic intervention window. These findings provide novel mechanistic insights and metabolic targets for therapeutic strategies in VCI.
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