Evidence map›Paper›PMID 33972291›Full record

ArticleeNeuro

Templated α-Synuclein Inclusion Formation Is Independent of Endogenous Tau.

Lindsay E Stoyka, Casey L Mahoney, Drake R Thrasher, Drèson L Russell, Anna K Cook, Anner T Harris, Ashwin Narayanan, Tiara P Janado, David G Standaert, Erik D Roberson and 1 more

Open access · goldAbstract read
In one paragraph

Article in eNeuro. 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
1.3field-weighted citation impact, top 17% 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, 17 citations in OpenAlex.

  1. Article
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  9. Review
  10. Neuronopathic GBA1L444P Mutation Accelerates Glucosylsphingosine Levels and Formation of Hippocampal Alpha-Synuclein Inclusions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
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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

11 authors at 1 institution in 1 country.

Lindsay E StoykaCenter for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294.ORCID 0000-0002-6376-0109
Casey L MahoneyCenter for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294.ORCID 0000-0002-6142-3627
Drake R ThrasherCenter for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294.
Drèson L RussellCenter for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294.
Anna K CookCenter for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294.
Ashwin Narayanan
Tiara P Janado
David G StandaertORCID 0000-0003-2921-8348
Laura A Volpicelli-DaleyCenter for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294 lvolpicellidaley@uabmc.edu.ORCID 0000-0001-8934-4018
University of Alabama at Birmingham · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008361 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YACOUBIAN, TALENE ALENE · 1992 to 2024
$16.8M
Project 3: LRRK2 mediated macrophage responses in PDP50NS108675 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2018 to 2022
$9.9M
Role of presynaptic targeting of alpha-synuclein in the pathogenesis of Parkinson's Disease and Dementia with Lewy BodiesR01NS102257 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI VOLPICELLI-DALEY, LAURA A. · 2018 to 2022
$1.9M
Mechanisms for the Benefit of Tau Reduction in Alzheimer Disease ModelsR01NS075487 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROBERSON, ERIK D · 2011 to 2015
$1.6M
Alpha-synuclein aggregate induced synapse loss is a pathological event contributing to Lewy body dementiasR56NS117465 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI VOLPICELLI-DALEY, LAURA A. · 2020 to 2020
$769k
Contribution of the interaction between synuclein and tau in the pathophysiology of dementia with Lewy bodiesF30AG058458 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STOYKA, LINDSAY ELIZABETH · 2018 to 2021
$168k
EPA EPD15032NIA NIH HHS F30 AG058458NIGMS NIH HHS T32 GM008361NINDS NIH HHS P50 NS108675NINDS NIH HHS R01 NS075487NINDS NIH HHS R01 NS102257NINDS NIH HHS R56 NS117465
6 · The paper itself

Abstract

Synucleinopathies including Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are characterized by neuronal intracellular inclusions of α-synuclein. PD dementia (PDD) and DLB are collectively the second most common cause of neurodegenerative dementia. In addition to associated inclusions, Lewy body diseases (LBDs) have dopaminergic neurodegeneration, motor defects and cognitive changes. The microtubule-associated protein tau has been implicated in LBDs, but the exact role of the protein and how it influences formation of α-synuclein inclusions is unknown. Reducing endogenous tau levels is protective in multiple models of Alzheimer's disease (AD), tauopathies, and in some transgenic synucleinopathy mouse models. Recombinant α-synuclein and tau proteins interact

Indexed as

alpha-SynucleinParkinson DiseaseAnimalsDopaminergic NeuronsMiceMice, Transgenictau Proteinsalpha-SynucleinMapt protein, mousetau ProteinsdementiaLewyneurodegenerativeParkinson’s diseasesynucleintau

Identifiers

PMID33972291
PMCPMC8213444
OpenAlexW3163641486

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.