CHCHD2 links mitochondrial dysfunction and α-synuclein misfolding in Parkinson's disease.

Derek Narendra, Brent J Ryan

Abstract read

In one paragraph

Article in Trends in neurosciences, 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

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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.

Derek NarendraMitochondrial Biology and Neurodegeneration Unit, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: derek.narendra@nih.gov.

Brent J RyanOxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK; Kavli Institute for Nanoscience Discovery, University of Oxford, Oxford, UK. Electronic address: Brent.ryan@dpag.ox.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease comprises multiple biological subtypes and a heterogeneous clinical course. A recent study by Liao et al. identifies CHCHD2 mutations as a mitochondrial entry point that links metabolic dysfunction to α-synuclein pathology. These findings highlight how rare sporadiclike monogenic forms of Parkinson's disease may inform mechanistic and therapeutic stratification.

Indexed as

alpha-SynucleinDNA-Binding ProteinsMitochondriaMitochondrial ProteinsParkinson DiseaseTranscription FactorsAnimalsHumansMutationalpha-SynucleinCHCHD2 protein, humanDNA-Binding ProteinsMitochondrial ProteinsTranscription Factorsdisease stratificationdopaminergic neuronsmitochondrial metabolismneurodegenerationoxidative stressprotein aggregation

Identifiers

PMID41763921

DOI10.1016/j.tins.2026.02.002

PMCPMC13328052

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LicenceCC BY

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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.