ArticleMolecular psychiatry2026
Superior frontal and hippocampal structures associated with onset versus recurrence of mood disorders in monozygotic twins.
Article in Molecular 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mood disorders involve complex neurobiological trajectories, making it difficult to identify predictors of their onset and progression. This prospective study disentangled markers of vulnerability from markers of illness recurrence by leveraging monozygotic twins discordant for mood disorders. We followed 136 monozygotic twins (66 affected [AT], 39 high-risk, and 31 low-risk unaffected twins [UT]; mean age 37.4 ± 9.1 years; 69.9% females) for 7.1 ± 0.8 years after baseline MRI. Cox regression examined associations between regional neuroanatomy (bilateral hippocampus, precuneus, anterior cingulate volumes; superior frontal gyrus [SFG] thickness) and: (1) time-to-first onset (UT) or (2) time-to-recurrence (AT), adjusting for age, sex, intracranial volume, and symptoms. In UT, thinner bilateral SFG and smaller left precuneus were associated with greater onset risk (HR = 1.1, p < 0.04). These regions showed an approximately linear relationship across structural quartiles, with progressively higher 7-year episode-free probability from Q1 (lowest measures) to Q4 (highest measures). In contrast, in AT, smaller precuneus and bilateral hippocampal volumes predicted higher recurrence risk (HR = 1.1, p < 0.037), following a threshold-like pattern, with markedly higher 7-year risk of a mood episode for individuals in Q1 (lowest volume) compared to the higher quartiles (Q2-Q4). Our findings indicate distinct neuroanatomical risk profiles: prefrontal thinning of SFG marks vulnerability to initial onset, potentially reflecting impaired cognitive control, while hippocampal atrophy predisposes to recurrence, possibly via stress-related neurotoxicity. These stage-specific biomarkers, identified under rigorous genetic control, highlight targeted prevention strategies: cognitive interventions preserving frontal integrity in high-risk populations, and hippocampal neuroprotection to sustain remission.
Identifiers
42337010What OpenQuestion 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 OpenQuestion graph.