# An MSA-P patient presenting with preserved glucose metabolism in the putamen, cerebellar hypometabolism and pronounced loss of presynaptic dopamine transporter in the striatum

**Authors:** Swen Hesse, Manja Schiefer, Solveig Tiepolt, Dorit Prochnow, Larissa Mämecke, Frank Hoffmann, Iñaki Schniewind, Osama Sabri, Björn Falkenburger, Sebastian Brock

PMC · DOI: 10.1186/s41824-026-00294-8 · 2026-03-20

## TL;DR

A patient with multiple system atrophy showed preserved glucose metabolism in the putamen and reduced metabolism in the cerebellum, suggesting a distinct subtype of synucleinopathy.

## Contribution

Identifies a distinct metabolic pattern in MSA that could represent a unique synucleinopathy subtype.

## Key findings

- Preserved glucose metabolism in the putamen was observed in an MSA patient.
- Significant cerebellar hypometabolism was detected alongside reduced presynaptic dopamine transporter in the striatum.
- Seed-amplification assay confirmed synucleinopathy, indicating a possible distinct subtype of MSA.

## Abstract

Positron emission tomography (PET) of the brain using [18F]fluorodeoxyglucose (FDG) is becoming increasingly important for the diagnosis and differential diagnosis of atypical parkinsonian syndrome such as multiple system atrophy (MSA), which is characterized by hypometabolism of the putamen, pons, and cerebellum. We report on a patient with clinically established MSA based on a rapidly progressive, poorly levodopa-responsive parkinsonian syndrome, multidomain autonomic failure, and imaging findings where hereditary spastic paraplegia was discussed as a differential diagnosis. PET images revealed a well-preserved glucose metabolism in the striatum, specifically in the putamen, while metabolism in the cerebellum was significantly reduced. This pattern of glucose metabolism might indicate a distinct subtype of synucleinopathy as proven by seed-amplification assay and should be taken into account when diagnosing patients with MSA.

## Linked entities

- **Chemicals:** [18F]fluorodeoxyglucose (PubChem CID 68614), FDG (PubChem CID 68614)
- **Diseases:** multiple system atrophy (MONDO:0007803), hereditary spastic paraplegia (MONDO:0019064)

## Full-text entities

- **Genes:** SNCA (synuclein alpha) [NCBI Gene 6622] {aka NACP, PARK1, PARK4, PD1}, LRRK2 (leucine rich repeat kinase 2) [NCBI Gene 120892] {aka AURA17, DARDARIN, PARK8, RIPK7, ROCO2}, SPAST (spastin) [NCBI Gene 6683] {aka ADPSP, FSP2, SPG4}, SPG16 (spastic paraplegia 16 (complicated, X-linked recessive)) [NCBI Gene 57760] {aka SPG}, SLC6A3 (solute carrier family 6 member 3) [NCBI Gene 6531] {aka DAT, DAT1, PKDYS, PKDYS1}
- **Diseases:** urinary urge incontinence (MESH:D053202), loss of smooth pursuit (MESH:D015835), gait ataxia (MESH:D020234), neurodegenerative disorder (MESH:D019636), spasticity (MESH:D009128), SAA (MESH:D009366), postural instability (MESH:D054972), rapid eye movement (REM) sleep behaviour disorder (MESH:D020187), striatonigral degeneration (MESH:D020955), HSP/SPG (MESH:D015419), MSA (MESH:D019578), Parkinson's disease (MESH:D010300), urinary incontinence (MESH:D014549), autonomic dysfunction (MESH:D001342), parkinsonian syndrome (MESH:D020734), bladder dysfunction (MESH:D001745), parkinsonism (MESH:D010302), MSA-P (MESH:C537381), hypophonic speech impairment (MESH:D013064), atrophy (MESH:D001284), HSP type 4 (MESH:C535697), non-synucleinopathies (MESH:D000080874), autonomic failure (MESH:D012791), ataxia (MESH:D001259), extrapyramidal-motor syndrome (MESH:D001480), orthostatic hypotension (MESH:D007024), cerebellar (MESH:D002526)
- **Chemicals:** glucose (MESH:D005947), levodopa (MESH:D007980), [123I]ioflupane (MESH:C519528), FDG (MESH:D019788)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13003084/full.md

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Source: https://tomesphere.com/paper/PMC13003084