Evidence map›Paper›PMID 41673920›Full record

Observational studyAlzheimer's research & therapy2026

Longitudinal changes of blood β-synuclein in cognitively unimpaired, mild cognitive impairment and sporadic Alzheimer´s disease.

Patrick Oeckl, Samir Abu-Rumeileh, Christopher M Weise, Markus Otto, Alzheimer’s Disease Neuroimaging Initiative

Abstract readObservational Study
In one paragraph

Observational study in Alzheimer's research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Patrick OecklDepartment of Neurology, Ulm University Hospital, Helmholtzstr. 8/1, Ulm, 89081, Germany.ORCID http://orcid.org/0000-0002-7652-7023
Samir Abu-RumeilehDepartment of Neurology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, Halle (Saale), 06120, Germany.ORCID http://orcid.org/0000-0003-0631-8506
Christopher M WeiseDepartment of Neurology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, Halle (Saale), 06120, Germany.
Markus OttoDepartment of Neurology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, Halle (Saale), 06120, Germany. markus.otto@uk-halle.de.ORCID http://orcid.org/0000-0003-4273-4267
Alzheimer’s Disease Neuroimaging Initiative

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundβ-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.

methodsIn 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.

resultsParticipants (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.

conclusionsOur 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.

Indexed as

Alzheimer Diseasebeta-SynucleinCognitive DysfunctionAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersCross-Sectional StudiesDisease ProgressionFemaleHumansLongitudinal StudiesMaleAmyloid beta-Peptidesbeta-SynucleinBiomarkersBlood biomarkerLongitudinal observationMild cognitive impairmentSporadic Alzheimer´s diseaseSynaptic degenerationβ-synuclein

Identifiers

PMID41673920
PMCPMC12930813

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.