Evidence map›Paper›PMID 33346120›Full record

ArticleNeuroscience2021

Dendritic Spine Remodeling and Synaptic Tau Levels in PS19 Tauopathy Mice.

Courtney K Walker, Kelsey M Greathouse, Benjamin D Boros, Emily H Poovey, Kelsey R Clearman, Raksha Ramdas, Hamad M Muhammad, Jeremy H Herskowitz

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Cadherin-13 Maintains Retinotectal Synapses via Transneuronal Interactions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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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

8 authors at 1 institution in 1 country.

Courtney K WalkerCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States.
Kelsey M GreathouseCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States.
Benjamin D BorosCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States.
Emily H PooveyCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States.
Kelsey R ClearmanCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States.
Raksha RamdasCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States.
Hamad M MuhammadCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States.
Jeremy H HerskowitzCenter for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, United States. Electronic address: jhersko@uab.edu.
University of Alabama at Birmingham · US

Funding

Systems Genetic Analysis of Cognitive Resilience Using Multi-Parent CrossesRF1AG063755 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KACZOROWSKI, CATHERINE COOK · 2019 to 2021
$7.2M
Identifying therapeutic targets that confer synaptic resilience to Alzheimer's diseaseR01AG061800 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Christopher A. Gaiteri, Jeremy H. Herskowitz · 2018 to 2026
$6.9M
Training Program in Cell, Molecular, and Developmental BiologyT32GM008111 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 1985 to 2022
$5.4M
UAB Research Training Program in Neurobiology of Cognition and Cognitive DisordersT32NS061788 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Farah Dominique Lubin · 2008 to 2026
$4.5M
Gene x Environment Interactions in Hypothalamic Dysfunction in Alzheimer's DiseaseRF1AG059778 · NIA · JACKSON LABORATORY · PI KACZOROWSKI, CATHERINE COOK, O'CONNELL, KRISTEN M · 2018 to 2020
$4.3M
Identifying the molecular systems, networks, and key molecules that underlie cognitive resilienceR01AG057911 · NIA · UPSTATE MEDICAL UNIVERSITY · PI GAITERI, CHRISTOPHER A. · 2017 to 2021
$3.8M
Targeting Rho Kinases for Alzheimer's disease TherapeuticsR01AG054719 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HERSKOWITZ, JEREMY H. · 2017 to 2021
$1.9M
Pathologic tau and dendritic spine loss in Alzheimer's diseaseF31AG067635 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WALKER, COURTNEY KAITLIN · 2020 to 2021
$75k
NIA NIH HHS F31 AG067635NIA NIH HHS R01 AG054719NIA NIH HHS R01 AG057911NIA NIH HHS R01 AG061800NIA NIH HHS RF1 AG063755NIGMS NIH HHS T32 GM008111NINDS NIH HHS T32 NS061788
6 · The paper itself

Abstract

Synapse or dendritic spine loss is the strongest correlate of cognitive decline in Alzheimer's disease (AD), and neurofibrillary tangles (NFTs), but not amyloid-β plaques, associate more closely with transition to mild cognitive impairment. Yet, how dendritic spine architecture is affected by hyperphosphorylated tau is still an ongoing question. To address this, we combined cell and biochemical analyses of the Tau P301S mouse line (PS19). Individual pyramidal neurons in the hippocampus and medial prefrontal cortex (mPFC) were targeted for iontophoretic microinjection of fluorescent dye, followed by high-resolution confocal microscopy and 3D morphometry analysis. In the hippocampus, PS19 mice and non-transgenic (NTG) littermates displayed equivalent spine density at 6 and 9 months, but both genotypes exhibited age-related thin spine loss. PS19 mice exhibited significant increases in synaptic tau protein levels and mean dendritic spine head diameter with age. This suggests that CA1 pyramidal neurons in PS19 mice may undergo spine remodeling in response to tau accumulation and age. In the mPFC, spine density was similar among PS19 mice and NTG littermates at 6 and 9 months, but age-related reductions in synaptic tau levels were observed among PS19 mice. Collectively, these studies reveal brain region-specific changes in dendritic spine density and morphology in response to age and the presence of hyperphosphorylated tau in the PS19 mouse line.

Indexed as

Alzheimer DiseaseDendritic SpinesTauopathiestau ProteinsAnimalsDisease Models, AnimalHippocampusMiceMice, Transgenictau Proteinsdendritic spinehippocampusprefrontal cortexsynapsetau

Identifiers

PMID33346120
PMCPMC8142378
OpenAlexW3113300735

What OpenQuestion holds

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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.