Evidence map›Paper›PMID 40551167›Full record

ArticleAlzheimer's research & therapy2025

Photobiomodulation mitigates blood-brain barrier disruption in APP/PS1 mouse model of Alzheimer's disease by activating the AMPK pathway.

Chunyan Ma, Yutong Ye, Xinyu Shi, Na Li, Zhiming Mu, Tao Tan, Huijuan Yin, Jianwu Dai, Yi Liu, Hongli Chen

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Chunyan MaState Key Laboratory of Separation Membranes and Membrane Processes & Key Laboratory of Hollow Fiber Membrane Materials and Membrane Processes, Tianjin Key Laboratory of Optoelectronic Detection Technology and Systems, Tiangong University, Tianjin, 300387, China.
Yutong YeState Key Laboratory of Separation Membranes and Membrane Processes & Key Laboratory of Hollow Fiber Membrane Materials and Membrane Processes, Tianjin Key Laboratory of Optoelectronic Detection Technology and Systems, Tiangong University, Tianjin, 300387, China.
Xinyu ShiState Key Laboratory of Separation Membranes and Membrane Processes & Key Laboratory of Hollow Fiber Membrane Materials and Membrane Processes, Tianjin Key Laboratory of Optoelectronic Detection Technology and Systems, Tiangong University, Tianjin, 300387, China.
Na LiState Key Laboratory of Separation Membranes and Membrane Processes & Key Laboratory of Hollow Fiber Membrane Materials and Membrane Processes, Tianjin Key Laboratory of Optoelectronic Detection Technology and Systems, Tiangong University, Tianjin, 300387, China.
Zhiming MuDepartment of Radiology, Tianjin Medical University General Hospital, No. 154, Anshan Road, Heping District, Tianjin, 300052, China.
Tao TanOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, Zhejiang Provincial Clinical Research Center for Mental Disorders, The Affiliated Wenzhou Kangning Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Huijuan YinState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Neuromodulation and Neurorepair, Integrative Regeneration Laboratory, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300192, China.
Jianwu DaiState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Neuromodulation and Neurorepair, Integrative Regeneration Laboratory, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300192, China.
Yi LiuState Key Laboratory of Separation Membranes and Membrane Processes & Key Laboratory of Hollow Fiber Membrane Materials and Membrane Processes, Tianjin Key Laboratory of Optoelectronic Detection Technology and Systems, Tiangong University, Tianjin, 300387, China.
Hongli ChenState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Neuromodulation and Neurorepair, Integrative Regeneration Laboratory, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300192, China. chenhli0107@163.com.

Funding

Oujiang Laboratory No. OJQD2022002The Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences No. 2021-I2M-1-058The National Key R&D Program of China No. 2023YFC2412502The National Key R&D Program of China No. 2024YFC3505503The National Natural Science Foundation of China No. 62175261The Natural Science Foundation of Hebei Province No. F2024110001Wenzhou Science and Technology Projects No. ZY2023006
6 · The paper itself

Abstract

backgroundPhotobiomodulation (PBM), which utilizes specific light wavelengths to regulate cellular metabolism, signal transduction, and gene expression, has emerged as a promising intervention for enhancing cognitive function in Alzheimer's disease (AD). The blood-brain barrier (BBB) plays a critical role in protecting the central nervous system, and its dysfunction is a major contributor to AD pathogenesis. Although PBM has shown therapeutic potential, its effects on BBB integrity and the underlying mechanisms remain unclear.

methodsSix-month-old female APP/PS1 transgenic mice were subjected to PBM intervention (808 nm, 20 mW/cm

resultsPBM significantly improved cognitive deficits and anxiety-like behaviors in AD mice. It enhanced BBB integrity by upregulating the TJs Occludin, Claudin-5, and ZO-1, while also facilitating Aβ clearance via the low-density lipoprotein receptor-related protein 1 (LRP1) pathway and microglial phagocytosis, thereby reducing Aβ accumulation in the brain. Mechanistically, PBM attenuated apoptosis and mitochondrial oxidative stress while promoting mitochondrial energy metabolism. Notably, PBM markedly increased phosphorylated AMPK (p-AMPK) levels in the brains of AD mice. In vitro, the protective effects of PBM on BBB integrity were substantially diminished upon AMPK inhibition, confirming that PBM exerts its neuroprotective effects through the activation of the AMPK pathway.

conclusionThis study demonstrates that PBM enhances BBB integrity and mitigates Aβ pathology in AD mice by activating the AMPK signaling pathway, underscoring its potential as a novel, non-invasive therapeutic strategy for AD.

Indexed as

Alzheimer DiseaseAMP-Activated Protein KinasesBlood-Brain BarrierLow-Level Light TherapyAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalFemaleMiceMice, TransgenicPresenilin-1Signal TransductionAMP-Activated Protein KinasesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorPresenilin-1Alzheimer's diseaseAMPKBlood–Brain BarrierLow-density lipoprotein receptor-related protein 1Mitochondrial functionPhotobiomodulationβ-amyloid

Identifiers

PMID40551167
PMCPMC12183848

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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.