Evidence map›Paper›PMID 22438081›Full record

ArticleMolecular neurobiology2012

TUDCA, a bile acid, attenuates amyloid precursor protein processing and amyloid-β deposition in APP/PS1 mice.

Ana F Nunes, Joana D Amaral, Adrian C Lo, Maria B Fonseca, Ricardo J S Viana, Zsuzsanna Callaerts-Vegh, Rudi D'Hooge, Cecília M P Rodrigues

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04987671 (A Pharmacokinetic and Pharmacodynamic Study of AMX0035 in Patients With ALS), which is not on this map. Cited by 129 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 3 pooled it
3.9field-weighted citation impact, top 6% 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.

NCT04987671 phase1 / phase2unknown statusnot on this mapstarted 2021, after this paper: background citation

A Pharmacokinetic and Pharmacodynamic Study of AMX0035 in Patients With ALS

TypeinterventionalSponsorAmylyx Pharmaceuticals Inc.Ran2021 to 2023Enrolled14ConditionsALSArmsAMX0035
3 · Its place in the literature

Who cites it

129 citing papers in PubMed, 3 syntheses or guidelines pooled it, 190 citations in OpenAlex.

  1. Pooled it
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  17. Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025
    Review
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69 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Ana F NunesResearch Institute for Medicines and Pharmaceutical Sciences (iMed.UL), Faculty of Pharmacy, University of Lisbon, Lisbon, 1649-003, Portugal.
Joana D Amaral
Adrian C Lo
Maria B Fonseca
Ricardo J S Viana
Zsuzsanna Callaerts-Vegh
Rudi D'Hooge
Cecília M P Rodrigues
University of Lisbon · PTKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by accumulation of amyloid-β (Aβ) peptide in the hippocampus and frontal cortex of the brain, leading to progressive cognitive decline. The endogenous bile acid tauroursodeoxycholic acid (TUDCA) is a strong neuroprotective agent in several experimental models of disease, including neuronal exposure to Aβ. Nevertheless, the therapeutic role of TUDCA in AD pathology has not yet been ascertained. Here we report that feeding APP/PS1 double-transgenic mice with diet containing 0.4 % TUDCA for 6 months reduced accumulation of Aβ deposits in the brain, markedly ameliorating memory deficits. This was accompanied by reduced glial activation and neuronal integrity loss in TUDCA-fed APP/PS1 mice compared to untreated APP/PS1 mice. Furthermore, TUDCA regulated lipid-metabolism mediators involved in Aβ production and accumulation in the brains of transgenic mice. Overall amyloidogenic APP processing was reduced with TUDCA treatment, in association with, but not limited to, modulation of γ-secretase activity. Consequently, a significant decrease in Aβ(1-40) and Aβ(1-42) levels was observed in both hippocampus and frontal cortex of TUDCA-treated APP/PS1 mice, suggesting that chronic feeding of TUDCA interferes with Aβ production, possibly through the regulation of lipid-metabolism mediators associated with APP processing. These results highlight TUDCA as a potential therapeutic strategy for the prevention and treatment of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAstrocytesBile Acids and SaltsBrainCognition DisordersDNA-Binding ProteinsHumansLipid MetabolismMiceMice, TransgenicMicrogliaNerve Tissue ProteinsNeuronsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAPP protein, humanBile Acids and SaltsDNA-Binding ProteinsNerve Tissue ProteinsNeuN protein, mouseNuclear ProteinsPresenilin-1SynucleinsTaurochenodeoxycholic Acidursodoxicoltaurine

Identifiers

PMID22438081
OpenAlexW2005971787

What OpenQuestion holds

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Registered trials

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.