Уровень белка p-tau217 в крови не является надежным маркером когнитивных нарушений при болезни Паркинсона без деменции

Plasma phosphorylated tau-217 (p-tau217) is not clearly associated with cognitive impairment among patients with Parkinson disease (PD) without dementia, according to study findings published in Movement Disorders. Researchers sought to determine whether plasma p-tau217, a biomarker of early Alzheimer disease (AD), is associated with cognitive impairment and domain-specific cognitive performance among patients with PD without dementia. The researchers analyzed data from the Quebec Parkinson Network, including patients with PD without dementia and healthy control participants. Plasma p-tau217 concentrations were measured in 223 participants, while glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) levels were available for a subset of 126 participants. Cognitive status was assessed using the Montreal Cognitive Assessment (MoCA), comprehensive neuropsychological testing across multiple cognitive domains, and patient-reported cognitive symptoms. Statistical models were adjusted for age, sex, education, and disease duration, with false discovery rate (FDR) correction applied for multiple comparisons. Overall, these findings suggest that p-tau217 alone is unlikely to fully capture [mild cognitive impairment] in PD, underscoring the need to consider both AD-related and PD-specific processes when investigating cognitive impairment in PD. The final cohort included 165 patients with PD and 58 healthy control participants. Patients with PD had a mean age of 66.0 years, with 112 of 165 patients being men, and mean disease duration was 6.7 years. Mean MoCA scores were lower among patients with PD than control participants (25.3 vs 27.1), and 77 patients with PD had MoCA scores below 26 compared with 12 control participants. Across detailed neuropsychological testing, the PD cohort performed worse than control participants on assessments of attention and working memory, executive function, memory, language, and visuospatial ability. Despite these differences in cognitive performance, plasma p-tau217, GFAP, and NfL concentrations did not differ significantly between groups after FDR correction. Mean plasma p-tau217 levels were 0.116 pg/mL in patients with PD and 0.122 pg/mL in control participants (P =.865). Within the PD cohort, higher p-tau217 concentrations were nominally associated with poorer visuospatial performance (P =.04), but the association did not remain significant after FDR correction. P-tau217 levels were also higher among patients with self-reported cognitive impairment (P =.03), although this difference did not remain significant after correction. Plasma p-tau217 was not associated with cognitive impairment defined by a MoCA score below 26 or with performance in attention and working memory, executive function, memory, or language. Similarly, an initial association between higher GFAP levels and poorer memory performance did not remain significant after FDR correction. The researchers also examined the influence of apolipoprotein E (APOE) ε4 carrier status. APOE ε4 carriers had significantly higher plasma p-tau217 concentrations than noncarriers after FDR correction (P =.014). However, APOE ε4 status was not associated with cognitive performance and did not modify the relationship between p-tau217 levels and cognitive outcomes after FDR correction. Additional analyses found no significant associations between p-tau217 or GFAP and overall PD severity. Higher NfL concentrations, however, were associated with worse patient-reported nonmotor symptoms and greater impairment in activities of daily living. Specifically, higher NfL levels were associated with worse Movement Disorder Society-Unified Parkinson’s Disease Rating Scale Part I scores (β=0.35; 95% CI, 0.10-0.60; P =.03) and Part II scores (β=0.39; 95% CI, 0.17-0.61; P =.006), but not Part III motor examination scores (P =.20). Study limitations include the inability to evaluate amyloid-β42/40 status, the lack of amyloid or tau positron emission tomography confirmation of Alzheimer disease pathology, the absence of validated PD-specific p-tau217 cutoffs, and the cross-sectional design. “Overall, these findings suggest that p-tau217 alone is unlikely to fully capture [mild cognitive impairment] in PD, underscoring the need to consider both AD-related and PD-specific processes when investigating cognitive impairment in PD,” the study authors concluded. Disclosures: This research was supported by the Fonds de Recherche du Québec–Santé, Healthy Brains for Healthy Lives, and Parkinson Canada. Multiple study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures. This article originally appeared on Neurology Advisor References: Kouchache T, Chan T, Sun S, et al. Association between plasma phosphorylated tau-217 and cognition in Parkinson’s disease. Mov Disord. Published online July 19, 2026. doi:10.1002/mds.70400