Evidence map›Paper›PMID 27385446›Full record

ArticleMolecular medicine (Cambridge, Mass.)2016

Resveratrol administration increases Transthyretin protein levels ameliorating AD features- importance of transthyretin tetrameric stability.

L M Santos, D Rodrigues, M Alemi, S C Silva, C A Ribeiro, I Cardoso

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 16% of its field
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  7. Resveratrol: Protective Agent Against Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2024
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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

6 authors at 2 institutions in 1 country.

L M SantosIBMC - Instituto de Biologia Celular e Molecular.
D RodriguesIBMC - Instituto de Biologia Celular e Molecular.
M AlemiIBMC - Instituto de Biologia Celular e Molecular.
S C SilvaIBMC - Instituto de Biologia Celular e Molecular.
C A RibeiroIBMC - Instituto de Biologia Celular e Molecular.
I CardosoIBMC - Instituto de Biologia Celular e Molecular.
Universidade do Porto · PTi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous in vivo work showed that resveratrol has beneficial effects in the AD pathology, resulting in increased expression of transthyretin (TTR). TTR binds Aβ peptide avoiding its aggregation and toxicity, and is reduced in the CSF and plasma, in AD. Further, resveratrol binds TTR, stabilizing the native TTR tetrameric structure. To further explore the mechanism of neuroprotection conferred by TTR in AD, resveratrol was administrated, in the diet, to 5-8 months old AD transgenic female mice carrying just one copy of the mouse TTR gene, for two months. Effects in brain Aβ burden were evaluated by immunohistochemistry, and in total brain Aβ levels by ELISA, showing a striking decrease in both parameters in treated animals. In addition, total brain LRP1 protein levels were increased in treated animals, although its gene expression was unaltered. To further understand the mechanism(s) underlying such improvement in AD features, we measured TTR plasma levels showing that TTR increased in resveratrol-treated mice, whereas liver TTR gene transcription was not altered. These results strengthen the stability hypothesis, which postulates that TTR is unstable in AD leading to accelerated clearance and lower levels. Therefore, resveratrol which stabilizes the TTR tetramer results in TTR normalized clearance, thus increasing the protein plasma levels. In turn, stabilized TTR binds more strongly to Aβ peptide, avoiding its aggregation. Our results represent a step forward to the understanding of the mechanism underlying TTR protection in AD and highlight the possibility of using TTR stabilization as a therapeutic target in AD.

Indexed as

A-Beta peptideAlzheimer’s Disease)LRP1NeuroprotectionTransthyretinTTR tetrameric stability

Identifiers

PMID27385446
PMCPMC5082299
OpenAlexW2478397531

What OpenQuestion holds

Textmetadata
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.