Evidence map›Paper›PMID 42897209›Full record

ArticleCommunications medicine2026

Phosphorylated tau 217 in young adults with Down syndrome and Down syndrome regression disorder.

Jonathan D Santoro, Sara Abdel-Latif, Abhik K Banerjee, Hannah Mager, Mackenzie Silverman, Lilia Kazerooni, Samuel T Otey, Mariam M Yousuf, Maeve C Lucas, Zinayida Schlachetzki and 2 more

Abstract read
In one paragraph

Article in Communications medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Jonathan D SantoroDivision of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA, USA. santoroj@usc.edu.ORCID http://orcid.org/0000-0002-8350-8234
Sara Abdel-LatifAlzheimer's Therapeutic Research Institute, University of Southern California, San Diego, CA, USA.
Abhik K BanerjeeDivision of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA, USA.
Hannah MagerNational Institutes of Health, Bethesda, MD, USA.
Mackenzie SilvermanDepartment of Neurology, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.
Lilia KazerooniDivision of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0009-0003-4147-5395
Samuel T OteyDivision of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0009-0000-2689-9841
Mariam M YousufDivision of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-1201-1546
Maeve C LucasDivision of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0009-0007-4802-3788
Zinayida SchlachetzkiAlzheimer's Therapeutic Research Institute, University of Southern California, San Diego, CA, USA.
Robert A RissmanDepartment of Neurology, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.
Michael S RafiiDepartment of Neurology, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0003-2640-2094

Funding

Non-invasive biometric screening for cerebrovascular disorders in persons with Down syndrome.K23HL155898 · NHLBI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI SANTORO, JONATHAN DOUGLAS · 2021 to 2025
$1.3M
NHLBI NIH HHS K23 HL155898U.S. Department of Health & Human Services | National Institutes of Health (NIH) K23HL155898
6 · The paper itself

Abstract

backgroundDown syndrome regression disorder (DSRD) causes a rapid loss of cognitive, behavioral, and daily living skills, usually in adolescents and young adults with Down syndrome. Because people with Down syndrome have a high lifetime risk of Alzheimer's disease, we examined whether DSRD is associated with an Alzheimer-related pattern of tau pathology.

methodsIn this prospective, single-center study, we measured plasma phosphorylated tau-217 (p-tau217), a blood marker of Alzheimer pathology, in 132 participants: 48 with DSRD, 39 with Down syndrome without regression (DSwR), and 45 neurodevelopmental controls. We compared p-tau217 concentrations across groups and examined relationships with demographic factors, medical conditions, treatment status, and diagnostic test abnormalities.

resultsMedian p-tau217 concentrations were similar in the DSRD (0.082 pg/mL), DSwR (0.084 pg/mL), and neurodevelopmental control (0.080 pg/mL) groups (overall comparison, p  =  0.57). Pairwise comparisons and models accounting for demographic and clinical factors also showed no statistically significant group differences. Among participants with DSRD, p-tau217 was not associated with treatment status or abnormalities on brain-wave testing, neuroimaging, or cerebrospinal fluid analysis. No clinical or demographic factor remained associated with p-tau217 after accounting for the number of analyses performed.

conclusionsThese findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer's disease. However, a single blood measurement cannot exclude Alzheimer pathology in an individual. Longitudinal studies using several complementary biomarkers are needed.

Identifiers

PMID42897209
PMCPMC13680608

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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.