Evidence map›Paper›PMID 40753006›Full record

ArticleThe journal of prevention of Alzheimer's disease2025

The role of Tau, amyloid-β and neuroinflammation in the association between cognition and white matter hyperintensities in a southeast Asian cohort.

Gurveen Kaur Sandhu, Ashwati Vipin, Jacklyn Leonardo, Fatin Zahra Zailan, Pricilia Tanoto, Faith Phemie Hui En Lee, Xin Ying Sim, Smriti Ghildiyal, Yi Jin Leow, Shan Yao Liew and 4 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

14 authors.

Gurveen Kaur SandhuDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Ashwati VipinDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Jacklyn LeonardoDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Fatin Zahra ZailanDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Pricilia TanotoDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Faith Phemie Hui En LeeDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Xin Ying SimDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Smriti GhildiyalDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Yi Jin LeowDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Shan Yao LiewDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Gursimar BhallaDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Rasyiqah Binte Shaik Mohamed SalimDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Bocheng QiuDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore.
Nagaendran KandiahDementia Research Centre (Singapore), 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore; Neuroscience and Mental Health Programme, 11 Mandalay Road, Lee Kong Chian School of Medicine, Nanyang Technological University, 308232, Singapore; National Healthcare Group, 3 Fusionopolis Link, Nexus @ One-North,138543, Singapore. Electronic address: nagaendran_kandiah@ntu.edu.sg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundElevated Glial Fibrillary Acidic Protein (GFAP) is associated with increased Phosphorylated Tau 181 (pTau181) induced neurodegeneration in Alzheimer's Disease.

objectiveHowever, the role of GFAP and pTau181 in vascular/mixed dementias requires elucidation within the Southeast Asian context, where their burden is considerable.

designPopulation based cross-sectional study.

settingBiomarkers and Cognition Study, Singapore (BIOCIS).

participantsBaseline data from n = 583 (40.3 % male), non-demented but at risk, Southeast Asian community participants, were included in this analysis. All participants displayed cognitive symptoms on the Subjective Memory Complaints Questionnaire, although they may or may not have objective cognitive deficits and did not meet the criteria for dementia as per the DSM - 5.

methodsNeuropsychological assessments for executive function evaluation, volumetric White Matter Hyperintensities (WMH) measurement and plasma biomarker expression, were determined in non-demented but at risk, Southeast Asian research participants. Partial correlation analysis demonstrated variable associations. Simple moderation analysis revealed the ability for plasma biomarkers to influence the relationship between executive function and WMH.

resultsWMH burden positively correlated to Neurofilament-Light (NfL) and pTau181. Executive function and processing speed negatively correlated to WMH burden. GFAP positively correlated to pTau181 and negatively correlated to executive function. NfL, GFAP, pTau181, and Amyloid beta 42/Amyloid beta 40 (Aβ42/Aβ40) ratio independently moderated, the relationship between executive function/processing speed and WMH burden.

conclusionInflammatory mechanisms represented by GFAP were linked to tau pathology and WMH and also moderated the association between WMH on cognitive performance.

Indexed as

Amyloid beta-PeptidesCognitionNeuroinflammatory Diseasestau ProteinsWhite MatterAgedBiomarkersCohort StudiesCross-Sectional StudiesExecutive FunctionFemaleGlial Fibrillary Acidic ProteinHumansMagnetic Resonance ImagingMaleMiddle AgedAmyloid beta-PeptidesBiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinMAPT protein, humantau ProteinsAmyloid beta 42 / amyloid beta 40 ratio (Aβ42/Aβ40)Cerebral small vessel disease (CSVD)Cognitive and Neurodegenerative MeasuresGlial fibrillary acidic protein (GFAP)Neurofilament light (NfL)NeuroinflammationPhosphorylated tau 181 (pTau181)White Matter Hyperintensities (WMH)

Identifiers

PMID40753006
PMCPMC12501327

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.