Evidence map›Paper›PMID 40819213›Full record

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

Long-term impact of white matter hyperintensities and amyloid beta on thalamic subregions in cerebral small vessel disease: A prospective cohort study.

Zhenyu Cheng, Meng Li, Jing Li, Nan Zhang, Yena Che, Yiwen Chen, Pengcheng Liang, Yuanyuan Wang, Na Wang, Xinyue Zhang and 2 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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
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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

12 authors.

Zhenyu ChengKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Meng LiDepartment of Psychiatry and Psychotherapy, Jena University Hospital, Jena, Thuringia, Germany.
Jing LiDepartment of Radiology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua Medicine, Tsinghua University, Changping District, Beijing, China.
Nan ZhangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Yena CheDepartment of Medical Genetics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Yiwen ChenKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Pengcheng LiangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Yuanyuan WangCollege of Medical Imaging, Binzhou Medical University, Yantai, Shandong, China.
Na WangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Xinyue ZhangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Changhu LiangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Lingfei GuoKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.ORCID 0000-0002-4885-625X

Funding

Medical and Health Science and Technology Development Project of Shandong Province 202309010557Medical and Health Science and Technology Development Project of Shandong Province 202309010560Medical and Health Science and Technology Development Project of Shandong Province 202409010479Natural Science Foundation of China 82272072Natural Science Foundation of Shandong Province ZR2020MH288Natural Science Foundation of Shandong Province ZR2024MH026Shandong Province Medical System Employee Science and Technology Innovation Plan SDYWZGKCIH2023034Shandong Province Medical System Employee Science and Technology Innovation Plan SDYWZGKCJH2024021Technology Development Plan of Jinan 202328066
6 · The paper itself

Abstract

introductionCerebral small vessel disease (CSVD) contributes to cognitive decline, yet the impact of white matter hyperintensity (WMH) distribution and plasma amyloid beta (Aβ) on thalamic subregions remains unclear.

methodsIn this prospective study, 175 patients with CSVD and matched controls underwent high-resolution magnetic resonance imaging (MRI), plasma biomarker assessment, and cognitive testing. WMHs were segmented and categorized by spatial patterns. Thalamic subregions were parcellated using the THalamus Optimized Multi-Atlas Segmentation (THOMAS) framework. Mixed-effects models evaluated the longitudinal effects of WMH progression and plasma Aβ on thalamic subregional volumes.

resultsCSVD patients exhibited selective atrophy in left medial geniculate nucleus (MGN), mediodorsal-parafascicular (MD-Pf), and lateral geniculate nucleus (LGN), with volumes associated with processing speed and attentional control. Thalamic and basal ganglia WMH burden significantly predicted subregional atrophy. In CSVD, WMH progression dominated longitudinal thalamic degeneration. DISCUSSION: Distinct WMH spatial patterns and vascular factors drive thalamic subregional atrophy in CSVD, contributing to cognitive decline. HIGHLIGHTS: Patients with cerebral small vessel disease (CSVD) exhibit selective atrophy in thalamic subregions compared to healthy controls (HCs). Thalamic white matter hyperintensity (WMH) burden strongly predicts mediodorsal-parafascicular and lateral geniculate nucleus atrophy in patients with CSVD. Plasma amyloid beta dynamics differentially influence thalamic integrity in CSVD compared to HCs.

Indexed as

Amyloid beta-PeptidesCerebral Small Vessel DiseasesThalamusWhite MatterAgedAtrophyBiomarkersCognitive DysfunctionCohort StudiesDisease ProgressionFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedProspective StudiesAmyloid beta-PeptidesBiomarkersamyloid betacerebral small vessel diseasecognitive impairmentthalamus subregionswhite matter hyperintensities

Identifiers

PMID40819213
PMCPMC12358008

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.