Evidence map›Paper›PMID 28805003›Full record

ReviewBrain pathology (Zurich, Switzerland)2017

Protein astrogliopathies in human neurodegenerative diseases and aging.

Gabor G Kovacs, Virginia M Lee, John Q Trojanowski

Abstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
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

56 citing papers in PubMed.

  1. Article
  2. Using Brain Organoids to Explore Human Neurobiology.Cellular and molecular neurobiology · 2026
    Review
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  18. Neuropathology of Alzheimer's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  19. Article
  20. 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

3 authors.

Gabor G KovacsInstitute of Neurology, Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0003-3841-5511
Virginia M LeeCenter for Neurodegenerative Disease Research, Institute on Aging and Department of Pathology and Laboratory Medicine of the Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA.
John Q TrojanowskiCenter for Neurodegenerative Disease Research, Institute on Aging and Department of Pathology and Laboratory Medicine of the Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA.

Funding

Transgenic Mouse Models of Tau PathologiesP01AG017586 · NIA · UNIVERSITY OF PENNSYLVANIA · PI LEE, VIRGINIA M · 2000 to 2021
$37.3M
UPenn ADCC Biomarker CoreP30AG010124 · NIA · UNIVERSITY OF PENNSYLVANIA · PI XIE, SHARON XIANGWEN · 1991 to 2020
$35.1M
Neuropathological Characterization of 'CTE'R01NS094003 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI Douglas Hamilton Smith, William Stewart · 2016 to 2026
$5.1M
Identification of Endophenotypes in the Behavioral-Variant of Frontotemporal DemeK23NS088341 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI IRWIN, DAVID JOHN · 2014 to 2018
$836k
NIA NIH HHS P01 AG017586NIA NIH HHS P30 AG010124NINDS NIH HHS K23 NS088341NINDS NIH HHS R01 NS094003
6 · The paper itself

Abstract

Neurodegenerative diseases are characterized by progressive dysfunction and loss of neurons associated with depositions of pathologically altered proteins showing hierarchical involvement of brain regions. The role of astrocytes in the pathogenesis of neurodegenerative diseases is explored as contributors to neuronal degeneration or neuroprotection pathways, and also as potential mediators of the transcellular spreading of disease-associated proteins. Protein astrogliopathy (PAG), including deposition of amyloid-β, prion protein, tau, α-synuclein, and very rarely transactive response DNA-binding protein 43 (TDP-43) is not unprecedented or unusual in neurodegenerative diseases. Morphological characterization of PAG is considered, however, only for the neuropathological diagnosis and classification of tauopathies. Astrocytic tau pathology is seen in primary frontotemporal lobar degeneration (FTLD) associated with tau pathologies (FTLD-Tau), and also in the form of aging-related tau astrogliopathy (ARTAG). Importantly, ARTAG shares common features with primary FTLD-Tau as well as with the astroglial tau pathologies that are thought to be hallmarks of a brain injury-related tauopathy known as chronic traumatic encephalopathy (CTE). Supported by experimental observations, the morphological variability of PAG might reflect distinct pathogenic involvement of different astrocytic populations. PAG might indicate astrocytic contribution to spreading or clearance of disease-associated proteins, however, this might lead to astrocytic dysfunction and eventually contribute to the degeneration of neurons. Here, we review recent advances in understanding ARTAG and other related forms of PAG.

Indexed as

AgingAstrocytesBrainHumansNeurodegenerative Diseasestau ProteinsMAPT protein, humantau ProteinsA-betaalpha-synucleinARTAGastrocyteneurodegenerationPAGprionprion proteinprotein astrogliopathytauTDP-43

Identifiers

PMID28805003
PMCPMC5578412

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Registered trials

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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.