The triglyceride-glucose index in parkinsonian syndromes: a clinical dead end or a hint at central dysregulation?

28/08/2026

AI Summary

The TyG index does not reliably distinguish Parkinson's disease from atypical parkinsonism in this cohort.
Progressive supranuclear palsy patients showed significantly lower fasting glucose and markedly worse cognitive scores, suggesting a potential red flag for cognitive decline.
Further studies should include HOMA-IR and continuous glucose monitoring to clarify central metabolic dysregulation in parkinsonian syndromes.

AI Summary

AIM OF THE STUDY: This study assessed the triglyceride-glucose (TyG) index for differentiating between Parkinson's disease (PD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP), and its association with cognitive profiles and clinical status.

RESULTS: The TyG index did not differentiate PD from AP; however, PSP patients exhibited significantly lower fasting glucose levels than the PD and MSA groups (p < 0.05).

Cognitive function (Addenbrooke's Cognitive Examination III, ACE-III) was notably lower in PSP than in MSA and PD (p = 0.0019), especially in memory and fluency, while depressive symptoms (Beck Depression Inventory, BDI) remained similar (p = 1.0).

Basic summary

Neurol Neurochir Pol. 2026;60(4):482-486. doi: 10.5603/pjnns.112043.

ABSTRACT

AIM OF THE STUDY: This study assessed the triglyceride-glucose (TyG) index for differentiating between Parkinson’s disease (PD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP), and its association with cognitive profiles and clinical status.

MATERIAL AND METHODS: This retrospective cross-sectional study involved 329 patients (272 PD, 15 MSA, 42 PSP). Assessments included motor and non-motor symptoms, the TyG index, and metabolic profiles.

RESULTS: The TyG index did not differentiate PD from AP; however, PSP patients exhibited significantly lower fasting glucose levels than the PD and MSA groups (p < 0.05). The TyG index and lipid profiles did not differ significantly (p > 0.05) among the three groups. Cognitive function (Addenbrooke’s Cognitive Examination III, ACE-III) was notably lower in PSP than in MSA and PD (p = 0.0019), especially in memory and fluency, while depressive symptoms (Beck Depression Inventory, BDI) remained similar (p = 1.0).

CONCLUSIONS AND CLINICAL IMPLICATIONS: The TyG index is not a reliable method for differentiating PD from atypical parkinsonism. Lower fasting glucose levels in PSP serve as a potential “red flag” associated with cognitive decline. Future research should incorporate homeostatic model assessment of insulin resistance (HOMA-IR) and continuous glucose monitoring to further explore these metabolic associations.

PMID:42663389 | DOI:10.5603/pjnns.112043

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