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| Pàgina inicial > Articles > Articles publicats > Alpha-synuclein co-pathology in Down syndrome-associated Alzheimer's disease |
(Institut de Recerca Sant Pau) (Hospital Clínic i Provincial de Barcelona) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Fundació Catalana Síndrome de Down) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Ludwig-Maximilians-Universität München) (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Institut de Recerca Sant Pau) (Hospital Clínic i Provincial de Barcelona) (Institut de Recerca Sant Pau) (Ludwig-Maximilians-Universität München)
| Data: | 2025 |
| Resum: | Alpha-synuclein (αSyn) seed amplification assay (SAA) enables in vivo study of αSyn but remains underexplored in Down syndrome-associated Alzheimer's disease (DSAD). We analyzed αSyn-SAA in cerebrospinal fluid (CSF) from 270 adults with Down syndrome, from the Down Alzheimer Barcelona Neuroimaging Initiative and from the AD21 cohort from the Department of Neurology at the University Hospital, Ludwig Maximilian University of Munich, Germany. Neuropathological examinations were conducted in 19 brain donors (five with ante mortem CSF). Participants were classified as asymptomatic or symptomatic (prodromal/dementia) Alzheimer's disease (AD). CSF Aβ1-42/1-40, CSF and plasma p-Tau181, and neurofilament light chain (NfL) levels were measured. Neuropathological evaluations assessed AD neuropathological changes and Lewy body pathology (LBP). ΑSyn-SAA was positive in 9. 2% of cases, independent of age or cognitive status. Symptomatic αSyn-positive cases exhibited higher plasma NfL levels than αSyn-negative cases (31 vs 21 pg/mL, p = 0. 027). LBP was observed in 47% of necropsies. The individual with severe neocortical LBP was αSyn-SAA-positive. These findings highlight LBP prevalence in DSAD but suggest current SAA may fail to detect limited αSyn deposition. |
| Ajuts: | Instituto de Salud Carlos III PI18/00335 Instituto de Salud Carlos III PI22/00785 Instituto de Salud Carlos III PI18/00435 Instituto de Salud Carlos III PI22/00611 Instituto de Salud Carlos III PI14/1561 Instituto de Salud Carlos III PI20/01330 Instituto de Salud Carlos III PI22/00307 Instituto de Salud Carlos III PI20/01473 Instituto de Salud Carlos III PI23/01786 Instituto de Salud Carlos III CP24/00112 Instituto de Salud Carlos III CM22/00052 Instituto de Salud Carlos III CM22/00219 Instituto de Salud Carlos III CM22/00291 Instituto de Salud Carlos III CM22/00243 Instituto de Salud Carlos III CP20/00038 |
| Nota: | Altres ajuts: German Ministry of Research and Education; Deutsche Forschungsgemeinschaft, Grant/Award Number: EXC-2145-SyNergy---ID 390857198; Fondation Jérôme Lejeune, Grant/Award Number: 2326---GRT-2024A; Generalitat de Catalunya; Alzheimer's Association, Grant/Award Number: AARFD-21-852492 |
| Drets: | Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, i la comunicació pública de l'obra, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original. No es permet la creació d'obres derivades.  |
| Llengua: | Anglès |
| Document: | Article ; recerca ; Versió publicada |
| Matèria: | Alzheimer's disease ; Biomarker ; Down syndrome ; Lewy body pathology ; Neuropathology ; Seed amplification assay ; Α-synuclein |
| Publicat a: | Alzheimer's & dementia, Vol. 21 Núm. 6 (June 2025) , ISSN 1552-5279 |
