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47/100

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Down syndrome and Alzheimer's

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Introduction There is a need for early, objective markers of Alzheimer's disease (AD)-related synapse dysfunction in adults with Down syndrome (DS). The presynaptic protein β-synuclein is elevated in the blood of adults with DS. This study evaluates the positioning of these changes relative to changes in pathophysiological blood biomarkers along the AD continuum. Methods We quantified serum β-synuclein using immunoprecipitation-mass spectrometry in a cross-sectional cohort (n = 131) spanning the AD continuum in adults with DS (n = 88) and cognitively unimpaired euploid controls (n = 43). Results β-synuclein levels were elevated in individuals with DS (p Discussion These findings consolidate β-synuclein as an early blood-based biomarker of synaptic dysfunction and provide insight into early AD-related mechanisms.

What this study adds

Evidence grade: Moderate

This is a cross-sectional study of 131 participants. In this cross-sectional study of 131 people, serum beta-synuclein was elevated in adults with Down syndrome and is described as an early blood-based marker of synaptic dysfunction. It is a biomarker finding only and does not test any treatment, cure, or prevention.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Cervantes González, A., Morcillo-Nieto, A. O., Serrano, S., Benejam, B., Videla, L., Barroeta, I., et al. (2026). Changes in serum β-synuclein precede blood biomarkers of Alzheimer pathology in Down syndrome. Alzheimer's & dementia : the journal of the Alzheimer's Association. https://doi.org/10.1002/alz.71860

Vancouver

Cervantes González A, Morcillo-Nieto AO, Serrano S, Benejam B, Videla L, Barroeta I, et al. Changes in serum β-synuclein precede blood biomarkers of Alzheimer pathology in Down syndrome. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2026. doi:10.1002/alz.71860. PMID: 42768868.

BibTeX

@article{cervantesgonzalez2026-42768868,
  author  = {Cervantes González, A. and Morcillo-Nieto, A. O. and Serrano, S. and Benejam, B. and Videla, L. and Barroeta, I. and Fernández, S. and Del Hoyo Soriano, L. and others},
  title   = {{Changes in serum β-synuclein precede blood biomarkers of Alzheimer pathology in Down syndrome}},
  journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
  year    = {2026},
  doi     = {10.1002/alz.71860},
  pmid    = {42768868},
  url     = {https://doi.org/10.1002/alz.71860}
}

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How to read this study

Design: this is a cross-sectional study. Everyone is measured once, so it cannot show which came first. Read it as a snapshot of how two things go together at one moment.
Size: the record lists 131 participants. Ask whether that is enough for the question, and who they were.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded moderate. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Moderate means the abstract mentions a cohort, case-control or longitudinal design. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

Results β-synuclein levels were elevated in individuals with DS (p Discussion These findings consolidate β-synuclein as an early blood-based biomarker of synaptic dysfunction and provide insight into early AD-related mechanisms.

Why it matters

In this cross-sectional study of 131 people, serum beta-synuclein was elevated in adults with Down syndrome and is described as an early blood-based marker of synaptic dysfunction. It is a biomarker finding only and does not test any treatment, cure, or prevention.

Study details

Study designcross-sectional
Participants131
Evidence strengthModerate

How this study scored 47/100

Published in a leading specialty journal, and it is a snapshot of people at one point in time. Scored zero for effect reported and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	9 / 10	Tier 2 — leading specialty journal (Alzheimer's & dementia : the journal of the Alzheimer's Association)
Journal's citation record	2 / 4	Alzheimer s & Dementia: journal h-index 228 (OpenAlex, 2026-10-29)
Study design	4 / 12	A snapshot of people at one point in time
Strength of evidence	3 / 5	Rated “moderate” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	5 / 5	2026 — within 1 year(s) of the newest study here
Sample size	2 / 4	131 participants
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	0 / 7	Cited 0 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.0 citations a year over 2 year(s) since 2026
Impact for its field and year	0 / 6	Cited 0.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	0 / 6	No other study in this library cites it
Still being cited	0 / 4	Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Olivia Belbin: h-index 35 (OpenAlex, whole career)
Institution's track record	1 / 3	Universitat de Barcelona: institution h-index 1,049 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 9 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 42768868)
Free to read	2 / 2	Free to read
Total	47 / 100	—

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