| Home > In process > Longitudinal changes of blood β-synuclein in cognitively unimpaired, mild cognitive impairment and sporadic Alzheimer´s disease. > print |
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| 100 | 1 | _ | |a Oeckl, Patrick |0 P:(DE-2719)9001560 |b 0 |e First author |
| 245 | _ | _ | |a Longitudinal changes of blood β-synuclein in cognitively unimpaired, mild cognitive impairment and sporadic Alzheimer´s disease. |
| 260 | _ | _ | |a London |c 2026 |b BioMed Central |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a β-Synuclein is an emerging synaptic blood biomarker for Alzheimer´s disease (AD) and correlates with cognitive impairment, brain atrophy and amyloid/tau pathology. Longitudinal data from individual patients are missing so far but are important to evaluate how changes of β-synuclein might be used in early diagnosis, prediction, disease progression and treatment monitoring.In this observational study, we investigated serum β-synuclein by immunoprecipitation-mass spectrometry (IP-MS) in 463 participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) including clinically diagnosed cognitively unimpaired, mild cognitive impairment (MCI) and AD dementia subjects with ≥ 1 follow-up samples for 235 individuals and clinical follow-up for up to 19 years. CSF AD biomarker levels were available for 194 participants.Participants (40.0% female, n = 185) had a mean (± SD) age of 76.2 ± 6.7 years. The cross-sectional group comparison yielded higher β-synuclein levels in MCI and AD dementia compared with CU and in AD dementia vs MCI patients. Mean follow-up time of longitudinal serum samples was 2.3 ± 1.2 years. The longitudinal data indicate that β-synuclein levels are dynamic during all stages of the AD continuum (CU, MCI, dementia) with substantial inter-individual variation. β-Synuclein predicted MCI-to-dementia conversion and future cognitive decline and it performed better in discrimination of AD dementia patients than CSF neurogranin.Our longitudinal data support the use of serum β-synuclein levels for prediction of future cognitive decline and MCI-to-dementia conversion but needing confirmation. Further studies with biologically and clinically defined participants must verify the trajectories of β-synuclein during the AD continuum.The online version contains supplementary material available at 10.1186/s13195-026-01973-1. |
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| 650 | _ | 7 | |a Blood biomarker |2 Other |
| 650 | _ | 7 | |a Longitudinal observation |2 Other |
| 650 | _ | 7 | |a Mild cognitive impairment |2 Other |
| 650 | _ | 7 | |a Sporadic Alzheimer´s disease |2 Other |
| 650 | _ | 7 | |a Synaptic degeneration |2 Other |
| 650 | _ | 7 | |a β-synuclein |2 Other |
| 700 | 1 | _ | |a Abu-Rumeileh, Samir |0 0000-0003-0631-8506 |b 1 |
| 700 | 1 | _ | |a Weise, Christopher M |b 2 |
| 700 | 1 | _ | |a Otto, Markus |0 0000-0003-4273-4267 |b 3 |
| 700 | 1 | _ | |a Initiative, Alzheimer’s Disease Neuroimaging |b 4 |e Collaboration Author |
| 773 | _ | _ | |a 10.1186/s13195-026-01973-1 |g Vol. 18, no. 1, p. 45 |0 PERI:(DE-600)2506521-X |n 1 |p 45 |t Alzheimer's research & therapy |v 18 |y 2026 |x 1758-9193 |
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