Evidence map›Paper›PMID 40293716›Full record

ArticleInternational journal for numerical methods in biomedical engineering2025

Criterion for Assessing Accumulated Neurotoxicity of Alpha-Synuclein Oligomers in Parkinson's Disease.

Andrey V Kuznetsov

Abstract read
In one paragraph

Article in International journal for numerical methods in biomedical engineering, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
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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.

Andrey V KuznetsovDepartment of Mechanical and Aerospace Engineering, North Carolina State University, Raleigh, North Carolina, USA.

Funding

National Science Foundation
6 · The paper itself

Abstract

The paper introduces a parameter called "accumulated neurotoxicity" of α-syn oligomers, which measures the cumulative damage these toxic species inflict on neurons over time, given the years it typically takes for such damage to manifest. A threshold value for accumulated neurotoxicity is estimated, beyond which neuron death is likely. Numerical results suggest that rapid deposition of α-syn oligomers into fibrils minimizes neurotoxicity, indicating that the formation of Lewy bodies might play a neuroprotective role. Strategies such as reducing α-syn monomer production or enhancing degradation can decrease accumulated neurotoxicity. In contrast, slower degradation (reflected by longer half-lives of monomers and free aggregates) increases neurotoxicity, supporting the idea that impaired protein degradation may contribute to Parkinson's disease progression. Accumulated neurotoxicity is highly sensitive to the half-deposition time of free α-syn aggregates into fibrils, exhibiting a sharp increase as it transitions from negligible to elevated levels, indicative of neural damage.

Indexed as

alpha-SynucleinParkinson DiseaseHumansNeuronsalpha-SynucleinFinke‐WatzkyLewy bodymathematical modelingneuronα‐Synucleinopathy

Identifiers

PMID40293716
PMCPMC12036748

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.