Evidence map›Paper›PMID 30737468›Full record

ReviewLaboratory investigation; a journal of technical methods and pathology2019

Dissecting α-synuclein inclusion pathology diversity in multiple system atrophy: implications for the prion-like transmission hypothesis.

Jess-Karan S Dhillon, Jorge A Trejo-Lopez, Cara Riffe, Nikolaus R McFarland, Wesley M Hiser, Benoit I Giasson, Anthony T Yachnis

Open access · bronzeAbstract readReview
In one paragraph

Review in Laboratory investigation; a journal of technical methods and pathology, 2019. 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
2.3field-weighted citation impact, top 12% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Is Multiple System Atrophy a Prion-like Disorder?International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Current Management and Emerging Therapies in Multiple System Atrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
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

7 authors at 1 institution in 1 country.

Jess-Karan S DhillonDepartment of Neuroscience, University of Florida, Gainesville, FL, 32610, USA.
Jorge A Trejo-LopezCenter for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
Cara RiffeDepartment of Neuroscience, University of Florida, Gainesville, FL, 32610, USA.
Nikolaus R McFarlandCenter for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
Wesley M HiserDepartment of Pathology, University of Florida, Gainesville, FL, 32610, USA.
Benoit I GiassonDepartment of Neuroscience, University of Florida, Gainesville, FL, 32610, USA. bgiasson@ufl.edu.
Anthony T YachnisDepartment of Pathology, University of Florida, Gainesville, FL, 32610, USA. yachnis@pathology.ufl.edu.
University of Florida · US

Funding

University of Florida - Mt. Sinai Medical Center AD Research CenterP50AG047266 · NIA · UNIVERSITY OF FLORIDA · PI FEBO, MARCELO · 2015 to 2019
$7.3M
Interdisciplinary Training in Movement Disorders and NeurorestorationT32NS082168 · NINDS · UNIVERSITY OF FLORIDA · PI Melissa Jo Armstrong, David E Vaillancourt · 2015 to 2026
$2.8M
Prion and non-prion induction mechanisms of alpha-synuclein pathologyR01NS100876 · NINDS · UNIVERSITY OF FLORIDA · PI BORCHELT, DAVID R, GIASSON, BENOIT I · 2018 to 2022
$1.9M
Mechanisms of Aggregated Alpha-Synuclein Induction and ProgressionR01NS089622 · NINDS · UNIVERSITY OF FLORIDA · PI GIASSON, BENOIT I · 2014 to 2018
$1.6M
NIA NIH HHS P50 AG047266NINDS NIH HHS R01 NS089622NINDS NIH HHS R01 NS100876NINDS NIH HHS T32 NS082168
6 · The paper itself

Abstract

Synucleinopathies are a group of neurodegenerative diseases characterized by the accumulation of insoluble, aggregated α-synuclein (αS) pathological inclusions. Multiple system atrophy (MSA) presents with extensive oligodendroglial αS pathology and additional more limited neuronal inclusions while most of the other synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies (DLB), develop αS pathology primarily in neuronal cell populations. αS biochemical alterations specific to MSA have been described but thorough examination of these unique and disease-specific protein deposits is further warranted especially given recent findings implicating the prion-like nature of synucleinopathies perhaps with distinct strain-like properties. Taking advantage of an extensive panel of antibodies that target a wide range of epitopes within αS, we investigated the distinct properties of the various types of αS inclusion present in MSA brains with comparison to DLB. Brain biochemical fractionation followed by immunoblotting revealed that the immunoreactive profiles were significantly more consistent for DLB than for MSA. Furthermore, epitope-specific immunohistochemistry varied greatly between different types of MSA αS inclusions and even within different brain regions of individual MSA brains. These studies highlight the importance of using a battery of antibodies for adequate appreciation of the various pathology in this distinct synucleinopathy. In addition, it can be posited that if the spread of pathology in MSA undergoes prion-like mechanisms, "strains" of αS aggregated conformers must be inherently unstable and readily mutable, perhaps resulting in a more stochastic progression process.

Indexed as

alpha-SynucleinBrainHumansInclusion BodiesMultiple System Atrophyalpha-Synuclein

Identifiers

PMID30737468
PMCPMC7209695
OpenAlexW2911549451

What OpenQuestion holds

Textmetadata
LicenceTDM
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.