Seed amplification of released alpha-synuclein strains reveals genotype-specific differences in Parkinson's disease neurons.

Jessica Chedid, Yuan Tang, Kevin Law, Lachlan Thompson, Yann Gambin, Emma Sierecki, Nicolas Dzamko

Abstract read

In one paragraph

Article in Frontiers in aging neuroscience, 2026. 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

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

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

7 authors.

Jessica Chedid *Macquarie Medical School, Faculty of Health and Human Sciences, Macquarie University, Sydney, NSW, Australia.

Yuan Tang *School of Medical Sciences, Faculty of Medicine and Health, Brain and Mind Centre, University of Sydney, Sydney, NSW, Australia.

Kevin LawSchool of Medical Sciences, Faculty of Medicine and Health, Charles Perkins Centre, University of Sydney, Sydney, NSW, Australia.

Lachlan ThompsonSchool of Medical Sciences, Faculty of Medicine and Health, Charles Perkins Centre, University of Sydney, Sydney, NSW, Australia.

Yann GambinEMBL Australia Node for Single Molecule Science and School of Biomedical Sciences, Faculty of Medicine, The University of New South Wales, Sydney, NSW, Australia.

Emma SiereckiEMBL Australia Node for Single Molecule Science and School of Biomedical Sciences, Faculty of Medicine, The University of New South Wales, Sydney, NSW, Australia.

Nicolas DzamkoMacquarie Medical School, Faculty of Health and Human Sciences, Macquarie University, Sydney, NSW, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease is one of a group of diseases collectively termed α-synucleinopathies, all of which are characterized by abnormal accumulation of toxic α-synuclein (α-syn) assemblies which are thought to follow a prion-like propagation model and drive neuronal death. Both intrinsic strain properties and the genetic background of affected individuals are hypothesized to influence α-syn aggregate accumulation, propagation, and extracellular release. As such, the aim of this study is to characterize how different genetic backgrounds modulate α-syn aggregate accumulation and release in response to treatment with different α-syn strains. iPSC-derived neurons from five different groups were employed (healthy non-PD controls (NPC), idiopathic PD (iPD),

Indexed as

alpha-synucleinIPSCParkinson’s diseaseseed amplificationstrain

Identifiers

PMID42774389

DOI10.3389/fnagi.2026.1917981

PMCPMC13593840

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.