Evidence map›Paper›PMID 24874737›Full record

Trial reportCell death & disease2014

Role of alpha-synuclein in autophagy modulation of primary human T lymphocytes.

T Colasanti, M Vomero, C Alessandri, C Barbati, A Maselli, C Camperio, F Conti, A Tinari, C Carlo-Stella, L Tuosto and 5 more

Open access · goldAbstract readMulticenter StudyRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

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  10. The Roles ofFrontiers in cellular neuroscience · 2022
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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

15 authors at 5 institutions in 1 country.

T Colasanti1] Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy [2] Department of Medical Sciences, San Raffaele Institute Pisana, Rome, Italy.
M VomeroDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
C AlessandriLupus Clinic, Department of Internal Medicine, "La Sapienza" University, Rome, Italy.
C Barbati1] Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy [2] Department of Medical Sciences, San Raffaele Institute Sulmona, L'Aquila, Italy.
A MaselliDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
C CamperioIstituto Pasteur-Fondazione Cenci Bolognetti, Department of Biology and Biotechnology "C. Darwin", "La Sapienza" University, Rome, Italy.
F ContiLupus Clinic, Department of Internal Medicine, "La Sapienza" University, Rome, Italy.
A TinariDepartment of Technology and Health, Istituto Superiore di Sanità, Rome, Italy.
C Carlo-Stella1] Department of Oncology and Hematology, Humanitas Cancer Center, Humanitas Clinical and Research Center, Rozzano (MI), Italy [2] Department of Medical Biotechnology and Translational Medicine, University of Milan, Italy.
L TuostoIstituto Pasteur-Fondazione Cenci Bolognetti, Department of Biology and Biotechnology "C. Darwin", "La Sapienza" University, Rome, Italy.
D Benincasa1] Laboratory of Clinical and Behavioral Neurology, IRCCS Fondazione Santa Lucia, Rome, Italy [2] Movement Disorder Unit, Sant'Andrea Hospital "La Sapienza" University, Rome, Italy.
G ValesiniLupus Clinic, Department of Internal Medicine, "La Sapienza" University, Rome, Italy.
W Malorni1] Department of Medical Sciences, San Raffaele Institute Sulmona, L'Aquila, Italy [2] Department of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy.
M PierdominiciDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
E Ortona1] Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy [2] Department of Medical Sciences, San Raffaele Institute Sulmona, L'Aquila, Italy.
Istituto Superiore di Sanità · ITSapienza University of Rome · ITIstituto Pasteur · ITFondazione Santa Lucia · ITHumanitas University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been demonstrated that α-synuclein can aggregate and contribute to the pathogenesis of some neurodegenerative diseases and it is capable of hindering autophagy in neuronal cells. Here, we investigated the implication of α-synuclein in the autophagy process in primary human T lymphocytes. We provide evidence that: (i) knocking down of the α-synuclein gene resulted in increased autophagy, (ii) autophagy induction by energy deprivation was associated with a significant decrease of α-synuclein levels, (iii) autophagy inhibition by 3-methyladenine or by ATG5 knocking down led to a significant increase of α-synuclein levels, and (iv) autophagy impairment, constitutive in T lymphocytes from patients with systemic lupus erythematosus, was associated with abnormal accumulation of α-synuclein aggregates. These results suggest that α-synuclein could be considered as an autophagy-related marker of peripheral blood lymphocytes, potentially suitable for use in the clinical practice.

Indexed as

AutophagyAdultAgedalpha-SynucleinBiomarkersFemaleGene Knockdown TechniquesHumansLupus Erythematosus, SystemicMaleMiddle AgedT-Lymphocytesalpha-SynucleinBiomarkersSNCA protein, human

Identifiers

PMID24874737
PMCPMC4047919
OpenAlexW2057556822

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.