Evidence mapPaperPMID 40806201Full record

ReviewInternational journal of molecular sciences2025

Unraveling the Role of Autotaxin and Lysophosphatidic Acid in Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Potential.

Jesús García-de Soto, Mónica Castro-Mosquera, Jessica María Pouso-Diz, Alejandro Fernández-Cabrera, Mariña Rodríguez-Arrizabalaga, Manuel Debasa-Mouce, Javier Camino-Castiñeiras, Anxo Manuel Minguillón Pereiro, Marta Aramburu-Núñez, Daniel Romaus-Sanjurjo and 5 more

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jesús García-de SotoNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0003-1774-4922
Mónica Castro-MosqueraNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0009-0005-3590-002X
Jessica María Pouso-DizNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.
Alejandro Fernández-CabreraServicio de Neurología, Hospital Universitario Lucus Augusti, 27003 Lugo, Spain.ORCID 0000-0002-8383-163X
Mariña Rodríguez-ArrizabalagaNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0003-4399-8037
Manuel Debasa-MouceNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0001-9511-7399
Javier Camino-CastiñeirasNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.
Anxo Manuel Minguillón PereiroNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-9834-1457
Marta Aramburu-NúñezNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-1212-9851
Daniel Romaus-SanjurjoNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0001-7715-1956
José Manuel AldreyNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.
Robustiano Pego-ReigosaServicio de Neurología, Hospital Universitario Lucus Augusti, 27003 Lugo, Spain.
Juan Manuel Pías-PeleteiroNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.
Tomás SobrinoNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-9760-8690
Alberto OuroNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, Spain.ORCID 0000-0003-4359-1704

Funding

Biomedical Research Networking Center on Neurodegenerative Diseases CB22/05/00067Instituto de Salud Carlos III PI22/00938INTERREG Atlantic Area EAPA_791/2018_ NEUROATLANTIC projectINTER-REG V A España Portugal (POCTEP) 0624_2IQBIONEURO_6_EMarie Skłodowska-Curie grant agreement 101066444Xunta de Galicia IN607A2022/07
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β plaques, tau hyperphosphorylation, and chronic neuroinflammation. Emerging evidence suggests a crucial role of lipid signaling pathways in AD pathogenesis, particularly those mediated by autotaxin (ATX) and lysophosphatidic acid (LPA). ATX, an enzyme responsible for LPA production, has been implicated in neuroinflammatory processes, blood-brain barrier dysfunction, and neuronal degeneration. LPA signaling, through its interaction with specific G-protein-coupled receptors, influences neuroinflammation, synaptic plasticity, and tau pathology, all of which contribute to AD progression. This review synthesizes recent findings on the ATX/LPA axis in AD, exploring its potential as a biomarker and therapeutic target. Understanding the mechanistic links between ATX, LPA, and AD pathology may open new avenues for disease-modifying strategies.

Indexed as

Alzheimer DiseaseLysophospholipidsPhosphoric Diester HydrolasesAnimalsBiomarkersHumansLysophospholipase DSignal TransductionBiomarkerslysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesAlzheimer’s diseaseautotaxinlipid signalinglysophosphatidic acidneuroinflammationtau pathology

Identifiers

PMID40806201
PMCPMC12346116

What Socratic holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.