Evidence map›Paper›PMID 34733860›Full record

ReviewFrontiers in medicine2021

Alpha-Synuclein Aggregation in Parkinson's Disease.

E Srinivasan, G Chandrasekhar, P Chandrasekar, K Anbarasu, A S Vickram, Rohini Karunakaran, R Rajasekaran, P S Srikumar

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 2 pooled it
11.5field-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

120 citing papers in PubMed, 2 syntheses or guidelines pooled it, 207 citations in OpenAlex.

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  9. Serum L-ornithine-derived polyamines as indicators of Parkinson disease progression.Journal of neural transmission (Vienna, Austria : 1996) · 2026
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60 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

8 authors at 3 institutions in 2 countries.

E SrinivasanBioinformatics Lab, Department of Biotechnology, School of Bio Sciences and Technology, Vellore Institute of Technology (Deemed to be University), Vellore, India.
G ChandrasekharBioinformatics Lab, Department of Biotechnology, School of Bio Sciences and Technology, Vellore Institute of Technology (Deemed to be University), Vellore, India.
P ChandrasekarBioinformatics Lab, Department of Biotechnology, School of Bio Sciences and Technology, Vellore Institute of Technology (Deemed to be University), Vellore, India.
K AnbarasuDepartment of Bioinformatics, Saveetha School of Engineering, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, India.
A S VickramDepartment of Biotechnology, Saveetha School of Engineering, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, India.
Rohini KarunakaranUnit of Biochemistry, Faculty of Medicine, AIMST University, Bedong, Malaysia.
R RajasekaranBioinformatics Lab, Department of Biotechnology, School of Bio Sciences and Technology, Vellore Institute of Technology (Deemed to be University), Vellore, India.
P S SrikumarUnit of Psychiatry, Faculty of Medicine, AIMST University, Bedong, Malaysia.
Vellore Institute of Technology University · INAIMST University · MYSaveetha University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD), a neurodegenerative disorder characterized by distinct aging-independent loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) region urging toward neuronal loss. Over the decade, various key findings from clinical perspective to molecular pathogenesis have aided in understanding the genetics with assorted genes related with PD. Subsequently, several pathways have been incriminated in the pathogenesis of PD, involving mitochondrial dysfunction, protein aggregation, and misfolding. On the other hand, the sporadic form of PD cases is found with no genetic linkage, which still remain an unanswered question? The exertion in ascertaining vulnerability factors in PD considering the genetic factors are to be further dissevered in the forthcoming decades with advancement in research studies. One of the major proponents behind the prognosis of PD is the pathogenic transmutation of aberrant alpha-synuclein protein into amyloid fibrillar structures, which actuates neurodegeneration. Alpha-synuclein, transcribed by SNCA gene is a neuroprotein found predominantly in brain. It is implicated in the modulation of synaptic vesicle transport and eventual release of neurotransmitters. Due to genetic mutations and other elusive factors, the alpha-synuclein misfolds into its amyloid form. Therefore, this review aims in briefing the molecular understanding of the alpha-synuclein associated with PD.

Indexed as

alpha-synucleingenesmutationParkinson'sprotein aggregation

Identifiers

PMID34733860
PMCPMC8558257
OpenAlexW3206319754

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.