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Войти в исследования Neurologia i neurochirurgia polska · 2026
The triglyceride-glucose index in parkinsonian syndromes: a clinical dead end or a hint at central dysregulation?
СтатьяНазвание и аннотация: Перевод в очереди
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Buczek Aleksandra, Jaworska Emilia, Bigajski Hubert, Węgrzynek-Gallina Julia, Chmiela Tomasz, Siuda Joanna
Аннотация
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.
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.