Evidence map›Paper›PMID 40750516›Full record

ArticleThe journal of prevention of Alzheimer's disease2025

Differential effects of soluble and plaque amyloid on late-life depression: The moderating role of tau pathology.

Gihwan Byeon, Suhyung Kim, Sunghwan Kim, Yoo Hyun Um, Sheng-Min Wang, Seunggyun Ha, Sonya Youngju Park, Yeong Sim Choe, Donghyeon Kim, Hyun Kook Lim and 2 more

Abstract read
In one paragraph

Article in The journal of prevention of Alzheimer's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

12 authors.

Gihwan ByeonDepartment of Psychiatry, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea.
Suhyung KimDepartment of Psychiatry, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, 93 Jungbu-daero, Paldal-gu, Suwon-si, Gyeonggi-do 16247, Republic of Korea.
Sunghwan KimDepartment of Psychiatry, Yeouido St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 10 63-ro, Yeongdeungpo-gu, Seoul 07345, Republic of Korea.
Yoo Hyun UmDepartment of Psychiatry, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, 93 Jungbu-daero, Paldal-gu, Suwon-si, Gyeonggi-do 16247, Republic of Korea.
Sheng-Min WangDepartment of Psychiatry, Yeouido St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 10 63-ro, Yeongdeungpo-gu, Seoul 07345, Republic of Korea.
Seunggyun HaDivision of Nuclear Medicine, department of Radiology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea.
Sonya Youngju ParkDivision of Nuclear Medicine, Yeouido St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 10 63-ro, Yeongdeungpo-gu, Seoul 07345, Republic of Korea.
Yeong Sim ChoeResearch Institute, NEUROPHET Inc., 5F, 27 Teheran-ro 4-gil, Gangnam-gu, Seoul 06232, Republic of Korea.
Donghyeon KimResearch Institute, NEUROPHET Inc., 5F, 27 Teheran-ro 4-gil, Gangnam-gu, Seoul 06232, Republic of Korea.
Hyun Kook LimDepartment of Psychiatry, Yeouido St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 10 63-ro, Yeongdeungpo-gu, Seoul 07345, Republic of Korea; Research Institute, NEUROPHET Inc., 5F, 27 Teheran-ro 4-gil, Gangnam-gu, Seoul 06232, Republic of Korea; CMC Institute for Basic Medical Science, The Catholic Medical Center of The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea.
Chang Uk LeeDepartment of Psychiatry, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea.
Dong Woo KangDepartment of Psychiatry, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea. Electronic address: kato7@hanmail.net.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLate-life depression frequently co-occurs with Alzheimer's disease (AD); however, the interactive effects of amyloid-beta (Aβ) species and tau pathology on depressive symptoms remain unclear. Soluble oligomeric Aβ (OAβ) and amyloid plaques may differentially influence depression depending on tau burden.

objectivesTo examine how plasma OAβ and PET-measured amyloid plaque burden are associated with depressive symptoms across varying levels of tau pathology.

designCross-sectional analysis using generalized linear models with interaction terms, supported by stratified subgroup analyses and Johnson-Neyman procedures.

settingMemory disorder clinic at a university-affiliated hospital.

participantsA total of 103 individuals, including cognitively normal controls (n = 24), patients with mild cognitive impairment (n = 54), and amyloid-positive dementia (n = 25), all of whom underwent plasma biomarker testing and tau and amyloid PET imaging. MEASUREMENTS: Depression was evaluated using the Cornell Scale for Depression in Dementia (CSDD), Hamilton Depression Rating Scale (HAM-D), and Geriatric Depression Scale-Short Version (GDS-SV). Plasma OAβ was measured by Multimer Detection System (MDS), and PET quantified amyloid and tau burden.

resultsMDS-OAβ showed a significant negative interaction with tau PET SUVR on depression scores (FDR-adjusted p < 0.05). Higher OAβ levels were linked to greater depression severity in low-tau individuals, but inversely related in high-tau individuals. Amyloid plaque burden was associated with depression only in those with advanced tau pathology.

conclusionsThe association between amyloid pathology and depression differs depending on tau burden. Soluble OAβ may be a key contributor to depressive symptoms in early AD stages, while plaque effects become prominent later. These findings underscore the potential utility of OAβ as an early neuropsychiatric biomarker in AD and highlight the need to consider tau pathology when evaluating amyloid-related mood disturbances.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCognitive DysfunctionDepressionPlaque, Amyloidtau ProteinsAgedAged, 80 and overBiomarkersBrainCross-Sectional StudiesFemaleHumansMalePositron-Emission TomographyAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer diseaseAmyloid beta-peptidesDepressionTau proteins

Identifiers

PMID40750516
PMCPMC12501351

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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.