Evidence map›Paper›PMID 39251797›Full record

ArticleScientific reports2024

Microvascular and cellular dysfunctions in Alzheimer's disease: an integrative analysis perspective.

Mengjie Li, Xiaoyan Hao, Zhengwei Hu, Jie Tian, Jingjing Shi, Dongrui Ma, Mengnan Guo, Shuangjie Li, Chunyan Zuo, Yuanyuan Liang and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Vascular regeneration and blood flow recovery in glaucoma.Frontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. 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

14 authors.

Mengjie LiZhengzhou University, Zhengzhou, 450000, Henan, China.
Xiaoyan HaoZhengzhou University, Zhengzhou, 450000, Henan, China.
Zhengwei HuZhengzhou University, Zhengzhou, 450000, Henan, China.
Jie TianZhengzhou Railway Vocational and Technical College, Zhengzhou, 450000, Henan, China.
Jingjing ShiZhengzhou University, Zhengzhou, 450000, Henan, China.
Dongrui MaZhengzhou University, Zhengzhou, 450000, Henan, China.
Mengnan GuoZhengzhou University, Zhengzhou, 450000, Henan, China.
Shuangjie LiZhengzhou University, Zhengzhou, 450000, Henan, China.
Chunyan ZuoZhengzhou University, Zhengzhou, 450000, Henan, China.
Yuanyuan LiangZhengzhou University, Zhengzhou, 450000, Henan, China.
Mibo TangDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, 1 Jian-she East Road, Zhengzhou, 450000, Henan, China.
Chengyuan MaoDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, 1 Jian-she East Road, Zhengzhou, 450000, Henan, China.
Yuming XuDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, 1 Jian-she East Road, Zhengzhou, 450000, Henan, China.
Changhe ShiDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, 1 Jian-she East Road, Zhengzhou, 450000, Henan, China. shichanghe@zzu.edu.cn.

Funding

Funding for Scientific Research and Innovation Team of the First Affiliated Hospital of Zhengzhou University ZYCXTD2023011National Natural Science Foundation of China 81974211National Natural Science Foundation of China 82171247National Natural Science Foundation of China 82271277the Scientific and Technological Research Projects in Henan province 222102310033
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia, characterized by memory loss, cognitive decline, personality changes, and various neurological symptoms. The role of blood-brain barrier (BBB) injury, extracellular matrix (ECM) abnormalities, and oligodendrocytes (ODCs) dysfunction in AD has gained increasing attention, yet the detailed pathogenesis remains elusive. This study integrates single-cell sequencing of AD patients' cerebrovascular system with a genome-wide association analysis. It aims to elucidate the associations and potential mechanisms behind pericytes injury, ECM disorder, and ODCs dysfunction in AD pathogenesis. Finally, we identified that abnormalities in the pericyte PI3K-AKT-FOXO signaling pathway may be involved in the pathogenic process of AD. This comprehensive approach sheds new light on the complex etiology of AD and opens avenues for advanced research into its pathogenesis and therapeutic strategies.

Indexed as

Alzheimer DiseaseBlood-Brain BarrierGenome-Wide Association StudyPericytesExtracellular MatrixFemaleHumansMaleMicrovesselsOligodendrogliaPhosphatidylinositol 3-KinasesSignal TransductionSingle-Cell AnalysisPhosphatidylinositol 3-KinasesAlzheimer’s diseaseBlood–brain barrierGWASPI3K–AKT–FOXOScRNA-seq

Identifiers

PMID39251797
PMCPMC11385648

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.