Evidence map›Paper›PMID 30798354›Full record

ReviewActa neuropathologica2019

α-Synuclein and astrocytes: tracing the pathways from homeostasis to neurodegeneration in Lewy body disease.

Zachary A Sorrentino, Benoit I Giasson, Paramita Chakrabarty

Open access · greenAbstract readReview
In one paragraph

Review in Acta neuropathologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
14.3field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.

  1. Pooled it
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  15. Intercellular propagation of RIPK1/RIPK3 amyloid fibrils.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  20. Characterization of Isolated Human Astrocytes from Aging Brain.International journal of molecular sciences · 2025
    Article

38 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Zachary A SorrentinoDepartment of Neuroscience, Center for Translational Research in Neurodegenerative Diseases and McKnight Brain Institute, University of Florida, Gainesville, FL, 32610, USA.
Benoit I GiassonDepartment of Neuroscience, Center for Translational Research in Neurodegenerative Diseases and McKnight Brain Institute, University of Florida, Gainesville, FL, 32610, USA.
Paramita ChakrabartyDepartment of Neuroscience, Center for Translational Research in Neurodegenerative Diseases and McKnight Brain Institute, University of Florida, Gainesville, FL, 32610, USA. pchakrabarty@ufl.edu.ORCID 0000-0002-6226-3776
University of Florida · US

Funding

Mechanisms of Aggregated Alpha-Synuclein Induction and ProgressionR01NS089622 · NINDS · UNIVERSITY OF FLORIDA · PI GIASSON, BENOIT I · 2014 to 2018
$1.6M
Immune modulation and CNS pathology following exogenous α-synuclein challengeR21NS099738 · NINDS · UNIVERSITY OF FLORIDA · PI CHAKRABARTY, PARAMITA, GIASSON, BENOIT I · 2017 to 2018
$362k
NINDS NIH HHS R01 NS089622NINDS NIH HHS R21 NS099738
6 · The paper itself

Abstract

α-Synuclein is a soluble protein that is present in abundance in the brain, though its normal function in the healthy brain is poorly defined. Intraneuronal inclusions of α-synuclein, commonly referred to as Lewy pathology, are pathological hallmarks of a spectrum of neurodegenerative disorders referred to as α-synucleinopathies. Though α-synuclein is expressed predominantly in neurons, α-synuclein aggregates in astrocytes are a common feature in these neurodegenerative diseases. How and why α-synuclein ends up in the astrocytes and the consequences of this dysfunctional proteostasis in immune cells is a major area of research that can have far-reaching implications for future immunobiotherapies in α-synucleinopathies. Accumulation of aggregated α-synuclein can disrupt astrocyte function in general and, more importantly, can contribute to neurodegeneration in α-synucleinopathies through various pathways. Here, we summarize our current knowledge on how astrocytic α-synucleinopathy affects CNS function in health and disease and propose a model of neuroglial connectome altered by α-synuclein proteostasis that might be amenable to immune-based therapies.

Indexed as

alpha-SynucleinAnimalsAstrocytesHomeostasisHumansLewy Body DiseaseNeurodegenerative DiseasesNeuronsalpha-SynucleinAstrocyte heterogeneityExosomeGlial cytoplasmic inclusionLewy bodyNAC domainNeurodegenerationTherapyTransmissionTunneling nanotubeαSyn 3H11α-Synuclein

Identifiers

PMID30798354
PMCPMC6571045
OpenAlexW2917425115

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.