Evidence map›Paper›PMID 38625863›Full record

ArticlePloS one2024

Generating PET scan patterns in Alzheimer's by a mathematical model.

Chaeyoung Lee, Avner Friedman

Abstract read
In one paragraph

Article in PloS one, 2024. 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

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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

2 authors.

Chaeyoung LeeDepartment of Mathematics, Kyonggi University, Suwon, Republic of Korea.ORCID 0000-0002-1120-2455
Avner FriedmanDepartment of Mathematics, The Ohio State University, Columbus, OH, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer disease (AD) is the most common form of dementia. The cause of the disease is unknown, and it has no cure. Symptoms include cognitive decline, memory loss, and impairment of daily functioning. The pathological hallmarks of the disease are aggregation of plaques of amyloid-β (Aβ) and neurofibrillary tangles of tau proteins (τ), which can be detected in PET scans of the brain. The disease can remain asymptomatic for decades, while the densities of Aβ and τ continue to grow. Inflammation is considered an early event that drives the disease. In this paper, we develop a mathematical model that can produce simulated patterns of (Aβ,τ) seen in PET scans of AD patients. The model is based on the assumption that early inflammations, R and [Formula: see text], drive the growth of Aβ and τ, respectively. Recently approved drugs can slow the progression of AD in patients, provided treatment begins early, before significant damage to the brain has occurred. In line with current longitudinal studies, we used the model to demonstrate how to assess the efficacy of such drugs when given years before the disease becomes symptomatic.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHumansModels, TheoreticalPositron-Emission Tomographytau ProteinsAmyloid beta-Peptidestau Proteins

Identifiers

PMID38625863
PMCPMC11020767

What OpenQuestion holds

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Registered trials

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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.