Evidence map›Paper›PMID 40432308›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Prediction of longitudinal synaptic loss in Alzheimer's disease using tau PET and plasma biomarkers.

Jie Wang, Qi Huang, Xing Chen, Zhiwen You, Kun He, Xiaoxie Mao, Yiyun Huang, Nicolai Franzmeier, Michael Schöll, Tengfei Guo and 5 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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  10. Prediction of longitudinal synaptic loss in Alzheimer's disease using tau PET and plasma biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    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.

Jie WangDepartment of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0003-4338-2873
Qi HuangDepartment of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.
Xing ChenDepartment of Nuclear Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Zhiwen YouDepartment of Nuclear Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Kun HeDepartment of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.
Xiaoxie MaoDepartment of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.
Yiyun HuangPET Center, Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, Connecticut, USA.
Nicolai FranzmeierInstitute for Stroke and Dementia Research (ISD), LMU University Hospital, Ludwig-Maximilians-University (LMU), Munich, Germany.
Michael SchöllDepartment of Psychiatry and Neurochemistry, University of Gothenburg, The Sahlgrenska Academy, Institute of Neuroscience and Physiology, Gothenburg, Sweden.
Tengfei GuoInstitute of Biomedical Engineering, Shenzhen Bay Laboratory, Shenzhen, China.
Jun ZhaoDepartment of Nuclear Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yihui GuanDepartment of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.
Ruiqing NiInstitute for Biomedical Engineering, Institute for Regenerative Medicine, University of Zurich & ETH Zurich, Zurich; Department of Nuclear Medicine, Inselspital, Bern, Switzerland.
Binyin LiDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fang XieDepartment of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0003-2667-281X

Funding

National Science Foundation of China 81571345National Science Foundation of China 81801752National Science Foundation of China 8217052097National Science Foundation of China 82201583Shanghai Municipal Key Clinical Specialty 3030247006Shanghai Municipal Science and Technology Major Project 2018SHZDZX01Shanghai Sailing Program 18YF1403200Shanghai Sailing Program 19YF1405300startup fund of Huashan Hospital, Fudan University 2017QD081STI2030-Major Projects 2022ZD0213800ZJLab Clinical Research Plan of SHDC SHDC2020CR2056B
6 · The paper itself

Abstract

introductionWe investigated the associations of longitudinal synaptic loss and cognitive decline with tau burden and plasma biomarkers in Alzheimer's disease (AD).

methodsTwenty cognitively impaired (CI) individuals and 16 healthy controls (HC) underwent cognitive and plasma biomarker assessments, amyloid positron emission tomography (PET), tau PET, and synaptic density PET; after 1 year, tau and synaptic density PET were repeated. The relationships among tau burden, plasma biomarkers, synaptic density, and cognition were investigated.

resultsThe CI group had more longitudinal synapse loss and tau deposition than HCs. Longitudinal synaptic loss was positively associated with longitudinal cognitive decline, negatively with longitudinal tau deposition. Plasma glial fibrillary acidic protein (GFAP) mediates the relationship between longitudinal tau deposition and longitudinal synaptic loss. Tau burden, plasma phosphorylated tau181, and GFAP could predict longitudinal synaptic loss and cognitive decline.

conclusionsThe CI group had more longitudinal synapse loss and tau burden increases than HCs. Tau pathology and plasma GFAP could predict longitudinal synapse loss and cognitive decline. HIGHLIGHTS: Cognitively impaired individuals had more longitudinal synapse loss in the medial temporal lobe, and increased tau burden in the widespread neocortex than healthy controls. The longitudinal change of synaptic density was negatively associated with the longitudinal change of tau burden, and positively associated with longitudinal cognitive decline. Plasma glial fibrillary acidic protein (GFAP) mediates the relationship between longitudinal tau deposition and longitudinal synaptic loss. Tau burden, plasma phosphorylated tau181, and GFAP could predict longitudinal synaptic loss and cognitive decline.

Indexed as

Alzheimer DiseaseCognitive DysfunctionSynapsestau ProteinsAgedBiomarkersBrainFemaleGlial Fibrillary Acidic ProteinHumansLongitudinal StudiesMaleMiddle AgedPositron-Emission TomographyBiomarkersGlial Fibrillary Acidic ProteinMAPT protein, humantau Proteinscognitionlongitudinal synapse lossplasma glial fibrillary acidic proteinplasma phosphorylated tau 181synaptic densitytau burden

Identifiers

PMID40432308
PMCPMC12117192

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.