Cerebral metabolic trajectories alterations in multiple system atrophy: A longitudinal FDG-PET study.
Cerebral metabolic trajectories alterations in multiple system atrophy: A longitudinal FDG-PET study.
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Huashan, CN · Author affiliation
Department of Neurology, National Research Center for Aging and Medicine, National Center for Neurological Disorders, and State Key Laboratory of Brain Function and Disorders, Huashan Hospital, Fudan University, Shanghai, China.Location evidence
Shanghai, CN · Author affiliation
Department of Neurology, National Research Center for Aging and Medicine, National Center for Neurological Disorders, and State Key Laboratory of Brain Function and Disorders, Huashan Hospital, Fudan University, Shanghai, China.Location evidence
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Original abstract
Multiple system atrophy (MSA) is a rapidly progressive neurodegenerative disorder with different metabolic patterns in parkinsonian (MSA-P) and cerebellar (MSA-C) subtypes, but their longitudinal changes are not well understood. To characterize longitudinal changes of glucose metabolism and network connectivity in MSA using 18F-FDG-PET for early diagnosis and disease progression tracking, we retrospectively analyzed 29 MSA patients (17 MSA-P, 12 MSA-C) and 28 healthy controls. Regional glucose uptake was assessed as standardized uptake value ratios (SUVR). We examined inter-regional connectivity via correlation analysis and modeled metabolic decline using nonlinear mixed-effects models. Clinical progression was measured using the Unified Multiple System Atrophy Rating Scale (UMSARS). MSA-P displayed progressive hypometabolism in the putamen, cerebellum, and frontal cortex, while MSA-C showed declines primarily in the cerebellum and frontal regions. Longitudinal modeling indicated a faster putaminal decline in MSA-P (β = -0.015 ± 0.006) than in MSA-C (β = 0 ± 0.011), whereas cerebellar metabolism declined over time in both groups with overlapping slopes in MSA-P (β = -0.022 ± 0.006) and MSA-C (β = -0.022 ± 0.011). Regional metabolic reductions correlated with UMSARS progression (putamen in MSA-P: r = -0.59, p < 0.001; cerebellum in MSA-C: r = -0.62, p < 0.001). Significant connectivity disruptions were noted in frontal, basal ganglia, and cerebellar-parietal circuits. Longitudinal FDG-PET reveals distinct metabolic decline patterns in MSA subtypes-putamen in MSA-P and cerebellum in MSA-C-linked to clinical severity. These findings may inform clinical practice and trial design, supporting the use of FDG-PET for biological staging, monitoring disease progression, and potentially evaluating treatment responses.