Skip to content
PaperFren

Neurodegeneration

Does C9orf72 already change parietal EEG before ALS symptoms?

Dukic S, van Veenhuijzen K, Westeneng HJ, et al. · Human brain mapping · 2025

Open access · cc by · source: Europe PMC

In 87 asymptomatic relatives of C9orf72 ALS patients, carriers and non-carriers scored the same on a Go/NoGo attention task, but carriers showed stronger N2 negativity localized to precuneus and superior parietal cortex.

Save to libraryView originalAsk PaperFrenStudy this in NoteFren
Watch this

How this study connects

Role on claims

Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.

  • SupportsNeurodegenerative Biomarkersconcept

    The behavioural null is what makes the electrophysiological difference interesting.

    A signal can be detectable before any symptom or behavioural difference. Asymptomatic C9orf72 carriers showed no group difference across six sustained-attention metrics, while during the N2 window they showed a larger negative potential at central sensors localising to bilateral precuneus and superior parietal regions.

    Evidence for the claim as stated.

Study at a glance

Design
Case-control — Asymptomatic C9orf72 expansion carriers vs related non-carriers; high-density EEG during SART Go/NoGo, linear mixed models with pedigree
N
N=87 · 87 asymptomatic family members (37 C9+, 50 C9−) after excluding 12 of 99 recruited relatives
Population
Adult asymptomatic relatives of patients with familial C9orf72 ALS (UMC Utrecht, 2020–2024)
Outcome
Sensor- and source-space EEG (N2/P3 and response-locked) plus six SART behavioral measures

Structured fields used in claim comparison tables when every cited study has a complete layer.

Inspect source passages

Does C9orf72 already change parietal EEG before ALS symptoms?

These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.

87 asymptomatic family members: 37 C9+ and 50 C9−.

This study included 87 asymptomatic family members (AFM) of patients with familial C9orf72 ALS, comprising 37 individuals carrying the pathological repeat expansion (C9+) and 50 without it (C9−).

N2 window was 180–350 ms and P3 was 300–600 ms.

The stimulus‐locked Go and NoGo data were analysed within two time windows: 180–350 ms (N2) and 300–600 ms (P3)
Read passages in the original paper

Key findings

No group difference on six SART metrics. During N2, C9+ carriers had a larger negative potential at central sensors; source analysis localized this to bilateral precuneus and superior parietal regions, with response-locked data implicating the same posterior network.

Methodology

Recorded 128-channel BioSemi EEG at 512 Hz during SART in 37 C9+ and 50 C9− family members, analyzing stimulus-locked N2 (180–350 ms) and P3 (300–600 ms) plus response-locked ±100 ms windows with pedigree-aware linear mixed models.

Limitations

Cross-sectional EEG cannot prove these parietal changes predict conversion to ALS/FTD, and groups were not age-matched until sensitivity analyses; it is not a treatment or diagnostic-accuracy trial.

Related papers in this topic

Same topic cluster — not a recommendation engine.