Evidence map›Paper›PMID 23459573›Full record

ArticleFrontiers in pharmacology2013

Exploring the contribution of estrogen to amyloid-Beta regulation: a novel multifactorial computational modeling approach.

Thomas J Anastasio

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

Article in Frontiers in pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  6. Age-Dependent Sex Differences in Perineuronal Nets in anInternational journal of molecular sciences · 2023
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  18. When Does Alzheimer's Disease Really Start? The Role of Biomarkers.International journal of molecular sciences · 2019
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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

1 author at 1 institution in 1 country.

Thomas J AnastasioComputational Neurobiology Laboratory, Beckman Institute, Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign Urbana, IL, USA.
University of Illinois Urbana-Champaign · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

According to the amyloid hypothesis, Alzheimer Disease results from the accumulation beyond normative levels of the peptide amyloid-β (Aβ). Perhaps because of its pathological potential, Aβ and the enzymes that produce it are heavily regulated by the molecular interactions occurring within cells, including neurons. This regulation involves a highly complex system of intertwined normative and pathological processes, and the sex hormone estrogen contributes to it by influencing the Aβ-regulation system at many different points. Owing to its high complexity, Aβ regulation and the contribution of estrogen are very difficult to reason about. This report describes a computational model of the contribution of estrogen to Aβ regulation that provides new insights and generates experimentally testable and therapeutically relevant predictions. The computational model is written in the declarative programming language known as Maude, which allows not only simulation but also analysis of the system using temporal-logic. The model illustrates how the various effects of estrogen could work together to reduce Aβ levels, or prevent them from rising, in the presence of pathological triggers. The model predicts that estrogen itself should be more effective in reducing Aβ than agonists of estrogen receptor α (ERα), and that agonists of ERβ should be ineffective. The model shows how estrogen itself could dramatically reduce Aβ, and predicts that non-steroidal anti-inflammatory drugs should provide a small additional benefit. It also predicts that certain compounds, but not others, could augment the reduction in Aβ due to estrogen. The model is intended as a starting point for a computational/experimental interaction in which model predictions are tested experimentally, the results are used to confirm, correct, and expand the model, new predictions are generated, and the process continues, producing a model of ever increasing explanatory power and predictive value.

Indexed as

Alzheimer diseaseamyloid-βcomputational modeldeclarative programmingestrogenformal methodsmulti-drug therapymultifactorial process

Identifiers

PMID23459573
PMCPMC3585711
OpenAlexW2036165141

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.