Evidence map›Paper›PMID 35941704›Full record

ArticleActa neuropathologica communications2022

Corpora amylacea are associated with tau burden and cognitive status in Alzheimer's disease.

Connor M Wander, Tamy Harumy Moraes Tsujimoto, John F Ervin, Chanung Wang, Spencer M Maranto, Vanya Bhat, Julian D Dallmeier, Shih-Hsiu Jerry Wang, Feng-Chang Lin, William K Scott and 2 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  9. Polyglucosan body disease in an aged chimpanzee (Pan troglodytes).Neuropathology : official journal of the Japanese Society of Neuropathology · 2023
    Article
  10. Article
  11. Article
  12. Uncovering tau in wasteosomes (Frontiers in aging neuroscience · 2023
    Article
  13. Wasteosomes (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

12 authors at 4 institutions in 1 country.

Connor M WanderDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Tamy Harumy Moraes TsujimotoDepartment of Biostatistics, University of North Carolina, Chapel Hill, NC, USA.
John F ErvinBryan Brain Bank, Department of Neurology, Duke University School of Medicine, Durham, NC, USA.
Chanung WangDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA.
Spencer M MarantoDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Vanya BhatDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Julian D DallmeierBrain Endowment Bank, Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA.
Shih-Hsiu Jerry WangBryan Brain Bank, Department of Neurology, Duke University School of Medicine, Durham, NC, USA.
Feng-Chang LinDepartment of Biostatistics, University of North Carolina, Chapel Hill, NC, USA.
William K ScottBrain Endowment Bank, Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA.
David M HoltzmanDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA.
Todd J CohenDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. toddcohen@neurology.unc.edu.ORCID 0000-0002-4099-0278
University of North Carolina at Chapel Hill · USDuke University · USHope Center for Neurological Disorders · USUniversity of Miami · US

Funding

North Carolina Translational & Clinical Sciences Institute (NC TraCS)UL1TR001111 · NCATS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUSE, JOHN BERNARD, CAREY, TIMOTHY S · 2013 to 2017
$43.9M
Research Education Component CoreP30AG072958 · NIA · DUKE UNIVERSITY · PI Heather E. Whitson · 2021 to 2026
$24.1M
UNC Neuroscience Center Research Cores: MicroscopyP30NS045892 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZYLKA, MARK J. · 2003 to 2022
$11.5M
Preclinical CoreU54HD079124 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LI, YUN · 2013 to 2019
$8.0M
Effect of APOE on CNS Neurons: Role of LRPRF1NS090934 · NINDS · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2020 to 2025
$6.5M
Novel Strategies and Mechanisms to Target APOE and Alzheimer's DiseaseRF1AG047644 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M., HYMAN, BRADLEY T. · 2019 to 2019
$3.8M
Identifying Alzheimer’s Disease Causal Variants and Target Genes Using iPSC-derived MicrogliaR01AG066871 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COHEN, TODD JONATHAN, PHANSTIEL, DOUGLAS H. · 2020 to 2024
$3.7M
Dual CHIP Functions Control Tau Triage In Alzheimer's DiseaseR01AG061188 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COHEN, TODD JONATHAN, SCHISLER, JONATHAN C. · 2019 to 2023
$3.1M
NCATS NIH HHS UL1 TR001111NIA NIH HHS P30 AG072958NIA NIH HHS R01 AG061188NIA NIH HHS R01 AG066871NIA NIH HHS RF1 AG047644NICHD NIH HHS U54 HD079124NINDS NIH HHS P30 NS045892NINDS NIH HHS RF1 NS090934
6 · The paper itself

Abstract

Corpora amylacea (CA) and their murine analogs, periodic acid Schiff (PAS) granules, are age-related, carbohydrate-rich structures that serve as waste repositories for aggregated proteins, damaged cellular organelles, and other cellular debris. The structure, morphology, and suspected functions of CA in the brain imply disease relevance. Despite this, the link between CA and age-related neurodegenerative diseases, particularly Alzheimer's disease (AD), remains poorly defined. We performed a neuropathological analysis of mouse PAS granules and human CA and correlated these findings with AD progression. Increased PAS granule density was observed in symptomatic tau transgenic mice and APOE knock-in mice. Using a cohort of postmortem AD brain samples, we examined CA in cognitively normal and dementia patients across Braak stages with varying APOE status. We identified a Braak-stage dependent bimodal distribution of CA in the dentate gyrus, with CA accumulating and peaking by Braak stages II-III, then steadily declining with increasing tau burden. Refined analysis revealed an association of CA levels with both cognition and APOE status. Finally, tau was detected in whole CA present in human patient cerebrospinal fluid, highlighting CA-tau as a plausible prodromal AD biomarker. Our study connects hallmarks of the aging brain with the emergence of AD pathology and suggests that CA may act as a compensatory factor that becomes depleted with advancing tau burden.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EBrainCognitionHumansMicetau ProteinsAmyloid beta-PeptidesApolipoproteins Etau Proteins

Identifiers

PMID35941704
PMCPMC9361643
OpenAlexW4290643119

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.