Evidence map›Paper›PMID 41355756›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Modifying Glucose Metabolism Reverses Memory Defects of Alzheimer's Disease Model at Late Stages.

Fang Liu, Yiyu-Li Tang, Zong-Bo Zhang, Ya-Hong Tan, Si-Hui Lin, Ni-Ya Wang, Jin-Nan Li, Zhi-Jie Pan, Jian-Feng Li, Jing-Fei Huang and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Fang LiuKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Yiyu-Li TangYunnan Key Laboratory of Cell Metabolism and Disease, and Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, 650500, China.
Zong-Bo ZhangYunnan Key Laboratory of Cell Metabolism and Disease, and Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, 650500, China.
Ya-Hong TanKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Si-Hui LinKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Ni-Ya WangKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Jin-Nan LiKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Zhi-Jie PanKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Jian-Feng LiSchool of Chinese Materia Medica and Yunnan Key Laboratory of Southern Medicinal Utilization, Yunnan Chinese Medicine University, Kunming, 650500, China.
Jing-Fei HuangKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Yu-Qiang DingState Key Laboratory of Medical Neurobiology and MOF Frontiers Center for Brain Science, Institute of Brain Science, and Department of Laboratory Animal Science, Fudan University, Shanghai, 200032, China.
Chun-Ming GuoYunnan Key Laboratory of Cell Metabolism and Disease, and Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, 650500, China.
Lin XuKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Cheng PengYunnan Key Laboratory of Cell Metabolism and Disease, and Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, 650500, China.
Qi-Xin ZhouKey Laboratory of Animal Models and Human Disease Mechanisms, KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.ORCID https://orcid.org/0000-0003-1995-5846

Funding

National Natural Science Foundation of China 32070818National Natural Science Foundation of China 32071029National Natural Science Foundation of China 32170662National Natural Science Foundation of China 32271080National Natural Science Foundation of China 82473909National Program of Brain Science and Brain-Inspired Intelligence Technology 2030 2022ZD0204900Natural Science Foundation of Yunnan Province 202001BB050005The Lingang Laboratory LG-QS-202205-05Xingdian talent program of Yunnan ProvinceYunnan Fundamental Research Project 202401AS070131Yunnan Provincial Science and Technology Department 202402AA310014
6 · The paper itself

Abstract

Significant efforts have harvested a sophisticated understanding of Alzheimer's disease (AD) including amyloid beta (Aβ) cascade mechanisms, although effective treatment for reversing or stopping AD progression is not available. This study reports that ferul enanthate (SL), a novel derivative of active agents targeting brain microvessels, oxidative phosphorylation, and ATP generation can reverse the hippocampus-dependent spatial memory defects and reduce Aβ plaques in AD model mice (APP/PS1) at advanced stages. Spatial transcriptomics discovers that SL endows a cluster of genes expressing in Aging-AD-Rescue (AAR) pattern, which is prominent in hippocampal dendritic region where Aβ plaques are densely deposited. Furthermore, this AAR rule covers hippocampal Glut1 (glucose transporter 1) expression and ATP generation, which are further confirmed by immunoblotting or immunofluorescence studies. Our data demonstrate that SL can still reverse memory defects at advanced stages of AD mice by modifying aging-dependent multiple pathologies of AD, particularly promoting Glut1 expression and ATP generation.

Indexed as

Alzheimer DiseaseGlucoseMemory DisordersAmyloid beta-PeptidesAnimalsDisease Models, AnimalGlucose Transporter Type 1HippocampusHumansMiceMice, TransgenicAmyloid beta-PeptidesGlucoseGlucose Transporter Type 1agingAlzheimer's diseaseGlut1spatial transcriptomics

Identifiers

PMID41355756
PMCPMC12931168

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.