Work

Linking the cerebellum posterior lobules atrophy to multiple system atrophy cognitive impairment

Year: 2025

Type: article

Abstract: Cognitive impairments in multiple system atrophy (MSA) are linked to cerebellar dysfunction, but the role of specific posterior cerebellar lobules in domain-specific deficits remains unclear. Structural MRI and cognitive assessments were conducted in 108 MSA patients (59 MSA-C, 49 MSA-P) and 53 healthy controls. Cerebellar gray matter (GM) volumes were segmented using the Spatially Unbiased Infratentorial Toolbox (SUIT). Multivariate regression models tested associations between posterior lobule volumes and cognitive domain scores. MSA patients showed significant GM atrophy in cerebellar subregions VI-VIII compared to controls, with greater reductions in MSA-C than MSA-P. Cognitive deficits were observed in visuospatial function, executive abilities, attention, and working memory across the cohort. Regression analyses revealed distinct patterns: In the overall MSA group, Crus II atrophy predicted visuospatial impairment, while Lobule VIIIa atrophy explained executive dysfunction. In MSA-C, Crus II atrophy remained a significant predictor of visuospatial deficits, but no cerebellar-predictive relationships emerged in MSA-P. Posterior cerebellar subregions dissociable contribute to cognitive profiles in MSA. Crus II serves as a key substrate for visuospatial vulnerability, whereas Lobule VIIIa reflects executive network disruption. The absence of cerebellar predictors in MSA-P highlights subtype-specific mechanisms, suggesting non-cerebellar drivers of cognitive decline in this group. These findings underscore the need for targeted therapeutic strategies aligning with MSA subtype pathology. • Cerebellar posterior lobule GM structure contribute to visuospatial/executive function in MSA patients. • MSA patients , visuospatial dysfunction is linked to cerebellar subregion Crus II. • Gray matter atrophy in the posterior cerebellum lobule are associated with CI in MSA-C rather than MSA-P patients.

Source: Neurobiology of Disease

DOI: 10.1016/j.nbd.2025.107239