Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217
IntroductionPlasma phospho-tau 217 (pTau217) is a biomarker for Alzheimer’s disease (AD) pathology, reflecting amyloid (Aβ) and tau burden, but its role in Parkinson disease (PD) and 4-repeat(4R)-tauopathies remains incompletely understood. We measured plasma pTau217 across the cognitive spectrum of...
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Frontiers Media S.A.
2025-08-01
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| author | Giulia Musso Giulia Musso Eleonora Fiorenzato Valentina Misenti Simone Cauzzo Roberta Biundo Roberta Biundo Carmelo A. Fogliano Giulia Bonato Giulia Bonato Wassilios G. Meissner Wassilios G. Meissner Marta Campagnolo Miryam Carecchio Miryam Carecchio Francesca Vianello Andrea Guerra Andrea Guerra Chiara Cosma Annachiara Cagnin Annachiara Cagnin Diego Cecchin Diego Cecchin Martina Montagnana Angelo Antonini Angelo Antonini |
| author_facet | Giulia Musso Giulia Musso Eleonora Fiorenzato Valentina Misenti Simone Cauzzo Roberta Biundo Roberta Biundo Carmelo A. Fogliano Giulia Bonato Giulia Bonato Wassilios G. Meissner Wassilios G. Meissner Marta Campagnolo Miryam Carecchio Miryam Carecchio Francesca Vianello Andrea Guerra Andrea Guerra Chiara Cosma Annachiara Cagnin Annachiara Cagnin Diego Cecchin Diego Cecchin Martina Montagnana Angelo Antonini Angelo Antonini |
| author_sort | Giulia Musso |
| collection | DOAJ |
| description | IntroductionPlasma phospho-tau 217 (pTau217) is a biomarker for Alzheimer’s disease (AD) pathology, reflecting amyloid (Aβ) and tau burden, but its role in Parkinson disease (PD) and 4-repeat(4R)-tauopathies remains incompletely understood. We measured plasma pTau217 across the cognitive spectrum of Lewy body diseases (PD, Dementia with Lewy bodies [DLB]) and in 4R-tauopathies, comparing these groups to cognitively unimpaired (CU) and mild cognitive impairment (MCI) individuals.MethodsParticipants included 18 cognitively normal PD (PD-NC), 32 PD with MCI, and 7 PD with dementia (PDD), alongside 4 DLB patients, grouped as PDD/DLB. The 4R-tauopathy group included 28 Progressive Supranuclear Palsy (PSP) and 4 corticobasal syndrome (CBS) patients, compared to 51 CU and 26 MCI individuals. Ptau217 was measured using the fully automated Lumipulse platform, with values adjusted for creatinine levels. Further, the presence of AD-pathology was defined using a validated cut-off based on Aβ-PET.ResultsPTau217 levels were significantly lower in PD-NC and CU individuals compared to those with greater cognitive impairment (PD-MCI, PDD/DLB, and PSP/CBS), and MCI individuals. AD co-pathology was identified in 28% of PDD/DLB and PSP/CBS patients, 16% of PD-MCI, and none of PD-NC. MCI showed the highest pTau217 positivity (35%), while 8% of CU individuals were positive despite normal cognition. In PD, pTau217 negatively correlated with cognitive performance, as assessed by Montreal Cognitive Assessment (MoCA: rs = −0.38, p = 0.004) and Mini-Mental State Examination (MMSE: rs = −0.37, p = 0.006).DiscussionPlasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations. AD co-pathology independently contributes to cognitive deficits in PD, but not in PSP/CBS. |
| format | Article |
| id | doaj-art-6b92d082cfd24f3fba48691482b1095b |
| institution | Kabale University |
| issn | 1664-2295 |
| language | English |
| publishDate | 2025-08-01 |
| publisher | Frontiers Media S.A. |
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| series | Frontiers in Neurology |
| spelling | doaj-art-6b92d082cfd24f3fba48691482b1095b2025-08-20T04:01:26ZengFrontiers Media S.A.Frontiers in Neurology1664-22952025-08-011610.3389/fneur.2025.16388521638852Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217Giulia Musso0Giulia Musso1Eleonora Fiorenzato2Valentina Misenti3Simone Cauzzo4Roberta Biundo5Roberta Biundo6Carmelo A. Fogliano7Giulia Bonato8Giulia Bonato9Wassilios G. Meissner10Wassilios G. Meissner11Marta Campagnolo12Miryam Carecchio13Miryam Carecchio14Francesca Vianello15Andrea Guerra16Andrea Guerra17Chiara Cosma18Annachiara Cagnin19Annachiara Cagnin20Diego Cecchin21Diego Cecchin22Martina Montagnana23Angelo Antonini24Angelo Antonini25Department of Medicine–DIMED, University of Padua, Padua, ItalyLaboratory Medicine, University-Hospital of Padua, Padua, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyDepartment of General Psychology, University of Padova, Padua, ItalyIRCCS San Camillo, Via Alberoni, Venice, Lido, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyPadova Neuroscience Center (PNC), University of Padova, Padua, ItalyCHU Bordeaux, Service de Neurologie des Maladies Neurodégénératives, IMNc, Place Amélie Raba-Léon, Bordeaux, FranceUniv. de Bordeaux, CNRS, IMN, UMR, Bordeaux, FranceParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyPadova Neuroscience Center (PNC), University of Padova, Padua, ItalyComplex Operative Unit (UOC) of the Psychology, Neurology Hospital division, Padova University Hospital, Padua, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyPadova Neuroscience Center (PNC), University of Padova, Padua, ItalyDepartment of Medicine–DIMED, University of Padua, Padua, ItalyPadova Neuroscience Center (PNC), University of Padova, Padua, Italy0Department of Neuroscience, University of Padova, Padua, ItalyPadova Neuroscience Center (PNC), University of Padova, Padua, Italy1Nuclear Medicine Unit, Department of Medicine (DIMED), University of Padova, Padua, ItalyDepartment of Medicine–DIMED, University of Padua, Padua, ItalyParkinson and Movement Disorders Unit, Study Center for Neurodegeneration (CESNE), Department of Neuroscience, University of Padova, Padua, ItalyIRCCS San Camillo, Via Alberoni, Venice, Lido, ItalyIntroductionPlasma phospho-tau 217 (pTau217) is a biomarker for Alzheimer’s disease (AD) pathology, reflecting amyloid (Aβ) and tau burden, but its role in Parkinson disease (PD) and 4-repeat(4R)-tauopathies remains incompletely understood. We measured plasma pTau217 across the cognitive spectrum of Lewy body diseases (PD, Dementia with Lewy bodies [DLB]) and in 4R-tauopathies, comparing these groups to cognitively unimpaired (CU) and mild cognitive impairment (MCI) individuals.MethodsParticipants included 18 cognitively normal PD (PD-NC), 32 PD with MCI, and 7 PD with dementia (PDD), alongside 4 DLB patients, grouped as PDD/DLB. The 4R-tauopathy group included 28 Progressive Supranuclear Palsy (PSP) and 4 corticobasal syndrome (CBS) patients, compared to 51 CU and 26 MCI individuals. Ptau217 was measured using the fully automated Lumipulse platform, with values adjusted for creatinine levels. Further, the presence of AD-pathology was defined using a validated cut-off based on Aβ-PET.ResultsPTau217 levels were significantly lower in PD-NC and CU individuals compared to those with greater cognitive impairment (PD-MCI, PDD/DLB, and PSP/CBS), and MCI individuals. AD co-pathology was identified in 28% of PDD/DLB and PSP/CBS patients, 16% of PD-MCI, and none of PD-NC. MCI showed the highest pTau217 positivity (35%), while 8% of CU individuals were positive despite normal cognition. In PD, pTau217 negatively correlated with cognitive performance, as assessed by Montreal Cognitive Assessment (MoCA: rs = −0.38, p = 0.004) and Mini-Mental State Examination (MMSE: rs = −0.37, p = 0.006).DiscussionPlasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations. AD co-pathology independently contributes to cognitive deficits in PD, but not in PSP/CBS.https://www.frontiersin.org/articles/10.3389/fneur.2025.1638852/fullParkinson’s diseaseProgressive Supranuclear Palsymild cognitive impairmentpTau217amyloidtau |
| spellingShingle | Giulia Musso Giulia Musso Eleonora Fiorenzato Valentina Misenti Simone Cauzzo Roberta Biundo Roberta Biundo Carmelo A. Fogliano Giulia Bonato Giulia Bonato Wassilios G. Meissner Wassilios G. Meissner Marta Campagnolo Miryam Carecchio Miryam Carecchio Francesca Vianello Andrea Guerra Andrea Guerra Chiara Cosma Annachiara Cagnin Annachiara Cagnin Diego Cecchin Diego Cecchin Martina Montagnana Angelo Antonini Angelo Antonini Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217 Frontiers in Neurology Parkinson’s disease Progressive Supranuclear Palsy mild cognitive impairment pTau217 amyloid tau |
| title | Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217 |
| title_full | Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217 |
| title_fullStr | Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217 |
| title_full_unstemmed | Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217 |
| title_short | Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217 |
| title_sort | detecting amyloid and tau pathology in parkinson s disease 4r tauopathies and control subjects with plasma ptau217 |
| topic | Parkinson’s disease Progressive Supranuclear Palsy mild cognitive impairment pTau217 amyloid tau |
| url | https://www.frontiersin.org/articles/10.3389/fneur.2025.1638852/full |
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