Evidence map›Paper›PMID 40229453›Full record

ArticleScientific reports2025

Divergent neurodegeneration associations with choroid plexus volume and degree of calcification in cognitively normal APOE ε4 carriers and non-carriers.

Ilker Ozsahin, Xiuyuan Wang, Liangdong Zhou, Ke Xi, Seyed Hani Hojjati, Emily Tanzi, Thomas Maloney, Edward K Fung, Jonathan P Dyke, Kewei Chen and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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
  2. Article
  3. Article
  4. 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

21 authors.

Ilker OzsahinDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA. ilker.ozsahin@neu.edu.tr.
Xiuyuan WangDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Liangdong ZhouDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Ke XiDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Seyed Hani HojjatiDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Emily TanziDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Thomas MaloneyDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Edward K FungDepartment of Radiology, Weill Cornell Medicine, 525 East 68th Street, New York, NY, 10065, USA.
Jonathan P DykeDepartment of Radiology, Weill Cornell Medicine, 525 East 68th Street, New York, NY, 10065, USA.
Kewei ChenBanner Alzheimer Institute, Arizona State University, 901 E Willetta St, Phoenix, AZ, 85006, USA.
Silky PahlajaniDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Laura Beth McIntireDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Ana Paula CostaDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
William Jones DartoraDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Qolamreza R RazlighiDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Lidia GlodzikDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Yi LiDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Gloria C ChiangDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Henry RusinekDepartment of Radiology, New York University, 660 1st Avenue, New York, NY, 10016, USA.
Mony J de LeonDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA.
Tracy A ButlerDepartment of Radiology, Brain Health Imaging Institute, Weill Cornell Medicine, 407 East 61st Street, 2nd floor, New York, NY, 10065, USA. tab2006@med.cornell.edu.

Funding

CLINICAL RESEARCH TRAINING IN LATE-LIFE MOOD DISORDERST32MH019986 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HOWARD J AIZENSTEIN, Carmen Andreescu · 1997 to 2026
$6.9M
Spatial dysregulation of the lipidome in Alzheimers disease human and mouse brainR01AG078800 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI Laura Beth Johnson McIntire, Vilas Menon · 2022 to 2026
$3.3M
Acyl chain remodeling and regional lipid dysregulation in Alzheimer's diseaseR01AG072794 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI MCINTIRE, LAURA BETH JOHNSON · 2021 to 2025
$1.6M
NIA NIH HHS R01 AG072794NIA NIH HHS R01 AG078800NIMH NIH HHS T32 MH019986
6 · The paper itself

Abstract

Choroid plexus (CP), best known for producing CSF, also regulate inflammation and clear metabolic waste to maintain brain homeostasis. CP dysfunction is implicated in Alzheimer's Disease (AD), with MRI studies showing CP enlargement in AD. The basis for CP enlargement is unknown. We hypothesized that calcium deposition within CP, which increases with aging and in certain neurodegenerative conditions, might underlie pathologic CP enlargement and be linked to neurodegeneration. In 166 cognitively normal participants, we used multimodal imaging to examine CP structure (MRI-measured overall volume, CT-measured calcium volume), PET-measured Aβ, age, and APOE genotype as predictors of neurodegeneration, indexed as hippocampal volume. CP enlargement was associated with reduced hippocampal volume, particularly in APOE4 carriers. CP calcium was not independently associated with hippocampal volume. However, a significant interaction revealed APOE4 genotype-specific associations between CP calcium and neurodegeneration, with APOE4 carriers showing greater hippocampal volumes in association with greater CP calcium-opposite to our hypothesis. Results suggest that a factor other than calcium drives pathologic CP enlargement associated with neurodegeneration, with this factor especially important in APOE4 carriers. Candidate factors include lipids and inflammatory cells, which are known to accumulate in CP and be regulated by APOE. Our findings highlight CP as a critical locus for studying AD pathogenesis and the mechanisms by which APOE4 promotes AD.

Indexed as

Apolipoprotein E4CalcinosisChoroid PlexusNeurodegenerative DiseasesAgedAlzheimer DiseaseCalciumCognitionFemaleGenotypeHeterozygoteHippocampusHumansMagnetic Resonance ImagingMaleMiddle AgedApolipoprotein E4CalciumAPOECalcificationChoroid plexusNeurodegenerationPiB PET

Identifiers

PMID40229453
PMCPMC11997051

What OpenQuestion holds

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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.