Evidence map›Paper›PMID 31626288›Full record

ArticleJournal of neuropathology and experimental neurology2019

Astrocytic Tau Deposition Is Frequent in Typical and Atypical Alzheimer Disease Presentations.

Amber Nolan, Elisa De Paula Franca Resende, Cathrine Petersen, Kyra Neylan, Salvatore Spina, Eric Huang, William Seeley, Zachary Miller, Lea T Grinberg

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
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  6. Astrocyte and oligodendrocyte pathology in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  7. Review
  8. Article
  9. In situ seeding assay: A novel technique for direct tissue localization of bioactive tau.Journal of neuropathology and experimental neurology · 2024
    Article
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  11. Review
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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

9 authors at 1 institution in 2 countries.

Amber NolanDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
Elisa De Paula Franca ResendeDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
Cathrine PetersenDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
Kyra NeylanDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
Salvatore SpinaDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
Eric HuangDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
William SeeleyDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
Zachary MillerDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
Lea T GrinbergDepartment of Anatomic Pathology, University of California, San Francisco, CA; Memory and Aging Center, University of California, San Francisco, California; and Global Brain Health Institute based at University of California, San Francisco and Trinity College, Dublin, Ireland.
University of California, San Francisco · US

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
Neuropathological changes underlying clinical heterogeneity in Alzheimer diseaseK24AG053435 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRINBERG, LEA TENENHOLZ · 2016 to 2025
$1.8M
Neuropathological basis of brain network dysfunctionK08AG052648 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SPINA, SALVATORE · 2016 to 2020
$852k
NIA NIH HHS K08 AG052648NIA NIH HHS K24 AG053435NIA NIH HHS P01 AG019724NIA NIH HHS P50 AG023501
6 · The paper itself

Abstract

Typical Alzheimer disease (AD) features an amnestic syndrome that reflects the progression of pathology through specific neural networks. However, a subset of patients exhibits atypical onset with prominent language, behavioral, or visuospatial deficits that are not explained by current neuropathological staging schemes. Astrogliopathy featuring tau inclusions with thorn-shaped and granular fuzzy morphologies is common in the aging brain and collectively known as aging-related tau astrogliopathy (ARTAG). Prior studies have identified tau-positive thorn-shaped astrocytes in the white matter that associate with a primary progressive aphasia phenotype in an AD cohort. However, a possible contribution of ARTAG copathology to AD clinical heterogeneity has yet to be systematically examined. To investigate whether ARTAG pathology contributes to atypical presentations, we mapped the presence and density of ARTAG subtypes throughout cortical and subcortical regions in a well-characterized cohort of AD cases enriched for atypical presentations. In our cohort, ARTAG pathology is frequent and correlates with older age and higher Braak stage. ARTAG subtypes exhibit distinct distribution patterns with subpial and subependymal deposition occurring in the amygdala, while white and grey matter astrocytic deposition are distributed throughout cortical regions. However, ARTAG pathology is equally prevalent in cases with typical and atypical clinical presentations.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAstrocytesBrainFemaleGray MatterHumansMaleTauopathiestau ProteinsWhite MatterMAPT protein, humantau ProteinsAging-related tau astrogliopathy (ARTAG)AstrocytesAtypical Alzheimer diseaseClinical heterogeneityTau

Identifiers

PMID31626288
PMCPMC7967845
OpenAlexW2980716100

What OpenQuestion holds

Textmetadata
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.