ArticleTranslational psychiatry2026
Cerebellar hypermetabolism disrupts fronto-cerebellar resting-state functional connectivity and associated executive compensation.
Article 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebellar hypermetabolism measured with FDG-PET is interpreted as maladaptive plasticity, while increased cerebellar functional connectivity reported in fMRI studies indicates a compensatory role. Using Alcohol Use Disorder (AUD) as a neurobiological model, the combination of PET and fMRI examinations can extend our understanding of cerebellar mechanisms underlying brain reorganization within the fronto-thalamo-cerebellar circuit (FCC) supporting executive functions. The aim of the present study was to investigate resting-state functional connectivity (rs-FC) of the cerebellum and to examine its relationship with cerebellar metabolism, thalamic grey matter volume (GM) as a key node of the FCC, and executive functioning. In AUD patients, stronger negative rs-FC was found between the cerebellar lobule VIII seed and voxels in the left superior frontal gyrus compared with HC. Path analysis conducted in AUD patients indicated that cerebellar hypermetabolism was positively related to fronto-cerebellar rs-FC, and that fronto-cerebellar rs-FC was positively related to inhibition performance. In this model, after controlling for thalamic GM abnormalities, cerebellar hypermetabolism negatively impacted inhibition performance through rs-FC. Cerebellar hypermetabolism disrupts negative fronto-cerebellar rs-FC, resulting in desynchronization within the fronto-cerebellar loop that compromises compensation for executive deficits. Cerebellar hypermetabolism may represent a biomarker of alcohol-related brain dysfunction, as an initial mechanism in the cascade linking fronto-cerebellar desynchronization and executive impairment.
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.