ReviewTranslational psychiatry2026
Rethinking EEG biomarkers of brain disorders: a transdiagnostic dimensional view.
Review in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Developing clinically useful brain-based biomarkers remains a central challenge in translational psychiatry and neurology. Traditional approaches focusing on disorder-specific signals have shown limited clinical utility. EEG, a scalable and non-invasive measure of brain function, illustrates the value of an alternative perspective: transdiagnostic and dimensional biomarker development. Here, we use low-frequency activity (LFA) as an illustrative example to demonstrate this framework. We synthesize evidence from 176 EEG studies across chronic pain, migraine, fatigue, and depression and identify increased low-frequency activity (LFA) as the most consistent alteration across studies. Crucially, this absence of disorder specificity does not diminish its clinical value. Instead, it points to shared neural dysfunction, consistent with frameworks of thalamo-cortical dysrhythmia and excitation-inhibition imbalance. These processes may underlie shared symptom dimensions, such as negative affect, cognitive dysfunction, and somatic manifestations. Accordingly, such transdiagnostic, dimensional markers could support prevention, monitoring, stratification, and neuromodulation across disorders, exemplifying precision neuroscience via mechanistically grounded, clinically actionable biomarkers.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.