Evidence map›Paper›PMID 39548663›Full record

ReviewCNS neuroscience & therapeutics2024

Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.

Qian Yue, Xinyue Leng, Ningqing Xie, Zaijun Zhang, Deguang Yang, Maggie Pui Man Hoi

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

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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

6 authors.

Qian YueState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR, China.
Xinyue LengState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR, China.
Ningqing XieState Key Laboratory of Bioactive Molecules and Druggability Assessment, and Guangzhou Key Laboratory of Innovative Chemical Drug Research in Cardio-Cerebrovascular Diseases, and Institute of New Drug Research, Jinan University, Guangzhou, China.
Zaijun ZhangState Key Laboratory of Bioactive Molecules and Druggability Assessment, and Guangzhou Key Laboratory of Innovative Chemical Drug Research in Cardio-Cerebrovascular Diseases, and Institute of New Drug Research, Jinan University, Guangzhou, China.
Deguang YangDepartment of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Maggie Pui Man HoiState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR, China.

Funding

Fundamental Research Funds for the Central Universities 21623114National Natural Science Foundation of China 82061160374National Natural Science Foundation of China 82404892Natural Science Foundation of Guangdong Province 2024A1515012818The Science and Technology Development Fund (FDCT), Macau SAR 0023/2020/AFJThe Science and Technology Development Fund (FDCT), Macau SAR 0035/2020/AGJThe University of Macau Research Grant MYRG2022-00248-ICMSThe University of Macau Research Grant MYRG-CRG2022-00010-ICMS
6 · The paper itself

Abstract

Recent research has shown the presence of blood-brain barrier (BBB) breakdown in Alzheimer's disease (AD). BBB is a dynamic interface consisting of a continuous monolayer of brain endothelial cells (BECs) enveloped by pericytes and astrocytes. The restricted permeability of BBB strictly controls the exchange of substances between blood and brain parenchyma, which is crucial for brain homeostasis by excluding blood-derived detrimental factors and pumping out brain-derived toxic molecules. BBB breakdown in AD is featured as a series of BEC pathologies such as increased paracellular permeability, abnormal levels and functions of transporters, and inflammatory or oxidative profile, which may disturb the substance transportation across BBB, thereafter induce CNS disorders such as hypometabolism, Aβ accumulation, and neuroinflammation, eventually aggravate cognitive decline. Therefore, it seems important to protect BEC properties for BBB maintenance and neuroprotection. In this review, we thoroughly summarized the pathological alterations of BEC properties reported in AD patients and numerous AD models, including paracellular permeability, influx and efflux transporters, and inflammatory and oxidative profiles, and probably associated underlying mechanisms. Then we reviewed current therapeutic agents that are effective in ameliorating a series of BEC pathologies, and ultimately protecting BBB integrity and cognitive functions. Regarding the current drug development for AD proceeds extremely hard, this review aims to discuss the therapeutic potentials of targeting BEC pathologies and BBB maintenance for AD treatment, therefore expecting to shed a light on the future AD drug development by targeting BEC pathologies and BBB protection.

Indexed as

Alzheimer DiseaseBlood-Brain BarrierEndothelial CellsAnimalsHumansAlzheimer's diseaseBBB protectionblood–brain barrierinflux and efflux transporterparacellular permeabilityvascular inflammation

Identifiers

PMID39548663
PMCPMC11567945

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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.