Evidence map›Paper›PMID 36343257›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Aβ and tau prions feature in the neuropathogenesis of Down syndrome.

Carlo Condello, Alison M Maxwell, Erika Castillo, Atsushi Aoyagi, Caroline Graff, Martin Ingelsson, Lars Lannfelt, Thomas D Bird, C Dirk Keene, William W Seeley and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.3field-weighted citation impact, top 6% of its field
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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Alzheimer's Disease Research Center Down Syndrome Cores: Experience from two sites.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Guam ALS-PDC is a distinct double-prion disorder featuring both tau and Aβ prions.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Aβ and tau prions feature in the neuropathogenesis of Down syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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

13 authors at 6 institutions in 4 countries.

Carlo CondelloInstitute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.
Alison M MaxwellDepartment of Pharmaceutical Chemistry, University of California, San Francisco, CA 94158.
Erika CastilloInstitute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.ORCID 0000-0003-2492-901X
Atsushi AoyagiInstitute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.
Caroline GraffDepartment of Neurobiology, Care Sciences and Society, Karolinska Institute, Solna, Sweden 171 77.
Martin IngelssonDepartment of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden SE-751 05.
Lars LannfeltDepartment of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden SE-751 05.
Thomas D BirdDepartment of Medicine, Division of Medical Genetics, University of Washington, Seattle, WA 98195.
C Dirk KeeneDepartment of Laboratory Medicine and Pathology, University of Washington School of Medicine, Seattle, WA 98115.ORCID 0000-0002-5291-1469
William W SeeleyDepartment of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.ORCID 0000-0003-1410-2027
Daniel P PerlDepartment of Pathology (Neuropathology), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
Elizabeth HeadDepartment of Pathology and Laboratory Medicine, University of California, Irvine, CA 92697.
Stanley B PrusinerInstitute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.ORCID 0000-0003-1955-5498
University of California, San Francisco · USUniversity of Washington · USUppsala University · SEKarolinska University Hospital · SEUniformed Services University of the Health Sciences · USUniversity of California, Irvine · US

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
VIRAL DEGENERATIVE DEMENTING DISEASE IN AGING (SUPP)P01AG002132 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SALI, ANDREJ · 1985 to 2024
$51.7M
Furthering scientific understanding of mechanisms underlying resilience to the effects of AD pathology by incorporating state of the art quantification of gliosis, inflammation, & synaptic toxicityU01AG006781 · NIA · UNIVERSITY OF WASHINGTON · PI CRANE, PAUL K, LARSON, ERIC B · 1986 to 2020
$39.3M
Research Education ComponentP30AG062422 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Serggio Carlo Lanata · 2019 to 2026
$36.9M
University of Washington Alzheimer's Disease Research CenterP30AG066509 · NIA · UNIVERSITY OF WASHINGTON · PI SUMAN JAYADEV · 2020 to 2026
$29.0M
The Alzheimer's Disease Research Center at the University of California, IrvineP30AG066519 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI Crystal M. Glover · 2020 to 2026
$27.9M
PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
Adult Changes in Thought Study U01AG006781HHS | National Institutes of Health (NIH) P01AG002132HHS | NIH | National Institute on Aging (NIA) P30AG066519Medical Research CouncilNIA NIH HHS P01 AG002132NIA NIH HHS P01 AG019724NIA NIH HHS P30 AG062422NIA NIH HHS P30 AG066509NIA NIH HHS P30 AG066519NIA NIH HHS P50 AG023501NIA NIH HHS U01 AG006781UW Alzheimer's Disease Research Center P30AG066509
6 · The paper itself

Abstract

Down syndrome (DS) is caused by the triplication of chromosome 21 and is the most common chromosomal disorder in humans. Those individuals with DS who live beyond age 40 y develop a progressive dementia that is similar to Alzheimer's disease (AD). Both DS and AD brains exhibit numerous extracellular amyloid plaques composed of Aβ and intracellular neurofibrillary tangles composed of tau. Since AD is a double-prion disorder, we asked if both Aβ and tau prions feature in DS. Frozen brains from people with DS, familial AD (fAD), sporadic AD (sAD), and age-matched controls were procured from brain biorepositories. We selectively precipitated Aβ and tau prions from DS brain homogenates and measured the number of prions using cellular bioassays. In brain extracts from 28 deceased donors with DS, ranging in age from 19 to 65 y, we found nearly all DS brains had readily measurable levels of Aβ and tau prions. In a cross-sectional analysis of DS donor age at death, we found that the levels of Aβ and tau prions increased with age. In contrast to DS brains, the levels of Aβ and tau prions in the brains of 37 fAD and sAD donors decreased as a function of age at death. Whether DS is an ideal model for assessing the efficacy of putative AD therapeutics remains to be determined.

Indexed as

Alzheimer DiseaseDown SyndromePrionsAdultAmyloid beta-PeptidesBrainCross-Sectional StudiesHumanstau ProteinsAmyloid beta-PeptidesPrionstau ProteinsAβcellular bioassaysDown syndromeprionstau

Identifiers

PMID36343257
PMCPMC9674250
OpenAlexW4308430339

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.