Evidence map›Paper›PMID 41820479›Full record

ArticleScientific reports2026

Levels and instability of transthyretin and correlations with core biomarkers in Alzheimer's disease.

Tiago Gião, Miguel Tábuas-Pereira, Inês Baldeiras, Joana Saavedra, Alexandre Dias, Maria João Saraiva, Maria Rosário Almeida, Isabel Santana, Isabel Cardoso

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Tiago Giãoi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200- 135, Porto, Portugal.
Miguel Tábuas-PereiraFaculdade de Medicina, Universidade de Coimbra, 3000-075, Coimbra, Portugal.
Inês BaldeirasFaculdade de Medicina, Universidade de Coimbra, 3000-075, Coimbra, Portugal.
Joana Saavedrai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200- 135, Porto, Portugal.
Alexandre Diasi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200- 135, Porto, Portugal.
Maria João Saraivai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200- 135, Porto, Portugal.
Maria Rosário Almeidai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200- 135, Porto, Portugal.
Isabel SantanaFaculdade de Medicina, Universidade de Coimbra, 3000-075, Coimbra, Portugal. 7708@chuc.min-saude.pt.
Isabel Cardosoi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200- 135, Porto, Portugal. icardoso@ibmc.up.pt.

Funding

Fundação para a Ciência e a Tecnologia 2020.07444.BDFundação para a Ciência e a Tecnologia 2023.03111.BDFundação para a Ciência e a Tecnologia PTDC/MED-PAT/0959/2021Fundação para a Ciência e a Tecnologia UI/BD/153607/2022
6 · The paper itself

Abstract

Transthyretin (TTR) has gained attention due to its implication in Alzheimer's Disease (AD) by modulating amyloid-beta (Aβ) pathology. This study aimed to establish associations between TTR and key AD biomarkers, to enhance our understanding of the role of TTR in AD pathogenesis. We evaluated TTR levels and tetrameric instability in plasma and CSF in mild cognitive impairment (MCI-AD) and Dementia-AD patients examining associations with clinical, biochemical and genetic data. Plasma TTR levels were lower in Dementia-AD, especially in women. In the MCI-AD group, CSF TTR levels inversely correlated with markers of amyloid pathology and neurodegeneration such as Aβ40, p-Tau181, t-Tau and NfL. CSF TTR instability was negatively associated with CSF Aβ42, indicating an association with increased amyloid burden. In the whole cohort, plasma TTR instability correlated with CSF TTR instability. In line with the strong association between CSF TTR instability and Aβ42, we showed increased TTR instability in samples incubated with Aβ42. No significant associations were observed in the Dementia-AD group. This study emphasizes that TTR is associated with Aβ clearance and neurodegeneration. We propose Aβ42 and its increase in the brain as a factor destabilizing the TTR tetrameric fold, impairing TTR function.

Indexed as

Alzheimer DiseaseBiomarkersPrealbuminAgedAged, 80 and overAmyloid beta-PeptidesCognitive DysfunctionFemaleHumansMalePeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersPeptide FragmentsPrealbuminTTR protein, humanAlzheimer’s diseaseAmyloid-βBlood-based biomarkersInstabilityMCITransthyretin

Identifiers

PMID41820479
PMCPMC13100035

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.