Evidence map›Paper›PMID 41267644›Full record

ArticleAnnals of neurology2026

Anatomical Associations Between Focal Mitochondrial Metabolism and Patterns of Neurodegeneration in Amyotrophic Lateral Sclerosis.

Marlene Tahedl, We Fong Siah, Efstratios Karavasilis, Jennifer C Hengeveld, Mark A Doherty, Russell L McLaughlin, Orla Hardiman, Ee Ling Tan, Foteini Christidi, Jana Kleinerova and 1 more

Abstract read
In one paragraph

Article in Annals of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
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

11 authors.

Marlene TahedlComputational Neuroimaging Group (CNG), School of Medicine, Trinity College Dublin, Dublin, Ireland.
We Fong SiahComputational Neuroimaging Group (CNG), School of Medicine, Trinity College Dublin, Dublin, Ireland.
Efstratios KaravasilisSecond Department of Radiology, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Jennifer C HengeveldSmurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland.
Mark A DohertySmurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland.
Russell L McLaughlinSmurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland.
Orla HardimanComputational Neuroimaging Group (CNG), School of Medicine, Trinity College Dublin, Dublin, Ireland.
Ee Ling TanComputational Neuroimaging Group (CNG), School of Medicine, Trinity College Dublin, Dublin, Ireland.
Foteini ChristidiComputational Neuroimaging Group (CNG), School of Medicine, Trinity College Dublin, Dublin, Ireland.
Jana KleinerovaComputational Neuroimaging Group (CNG), School of Medicine, Trinity College Dublin, Dublin, Ireland.ORCID 0000-0001-8679-8516
Peter BedeComputational Neuroimaging Group (CNG), School of Medicine, Trinity College Dublin, Dublin, Ireland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAmyotrophic lateral sclerosis (ALS) has a very specific neuroimaging signature, but the molecular underpinnings of the strikingly selective anatomic involvement have not elucidated to date. Accordingly, a large neuroimaging study was conducted with 258 participants to evaluate associations between patterns of neurodegeneration and focal metabolic metrics.

methodsStructural and diffusivity alterations were systematically evaluated in a genetically stratified cohort. Voxelwise associations between neurodegeneration and physiological mitochondrial indices were systematically evaluated over the entire brain and also examined in specific regions.

resultsSignificant topological associations were identified between physiological mitochondria tissue density, nicotinamide adenine dinucleotide (NADH)-ubiquinone oxidoreductase, succinate dehydrogenase, cytochrome c oxidase (COX), mitochondrial respiratory capacity (MRC), tissue respiratory capacity (TRC), and propensity to focal atrophy in ALS. Anatomic correlations between mitochondrial metrics and morphometric change were particularly strong in GGGGCC hexanucleotide repeat carriers in C9orf72. Diffusivity analyses also confirmed associations between brain metabolism and microstructural degeneration. Higher focal mitochondria tissue density was associated with higher likelihood of frontal, temporal, cerebellar, opercular, thalamic, cingulum, putamen, corpus callosum, and corona radiata degeneration. Uncinate fasciculus degeneration was associated with higher Complex I, II, COX, and TRC activity. Topological associations were readily replicated in an external validation cohort.

interpretationOur data indicate that brain regions with high metabolic activity are particularly vulnerable to neurodegeneration in ALS. Anatomic associations between physiological cerebral metabolism and patterns of neurodegeneration implicate mitochondrial dysfunction in the pathophysiology of ALS. Although mitochondrial dysfunction may not be the primary etiological factor, it may represent a shared bottleneck of multiple converging molecular and genetic pathways, offering a potential opportunity for meaningful pharmacological intervention. ANN NEUROL 2026;99:614-628.

Indexed as

Amyotrophic Lateral SclerosisBrainMitochondriaAdultAgedC9orf72 ProteinCohort StudiesFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedC9orf72 Protein

Identifiers

PMID41267644
PMCPMC12954164

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.