Evidence map›Paper›PMID 26438087›Full record

ArticleMolecular and cellular biochemistry2016

Comparative analysis of four disease prediction models of Parkinson's disease.

Nadella Kumudini, Shaik Mohammad Naushad, Balraj Alex Stanley, Manoharan Niveditha, Gunasekaran Sharmila, Konda Kumaraswami, Rupam Borghain, Rukmini Mridula, Vijay Kumar Kutala

Abstract readComparative Study
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In one paragraph

Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 3 institutions in 1 country.

Nadella KumudiniDepartment of Biotechnology, Jawaharlal Nehru Technological University-Hyderabad, Hyderabad, India.
Shaik Mohammad NaushadSchool of Chemical and Biotechnology, SASTRA University, Tirumalaisamudram, Thanjavur, India.
Balraj Alex StanleySchool of Chemical and Biotechnology, SASTRA University, Tirumalaisamudram, Thanjavur, India.
Manoharan NivedithaSchool of Chemical and Biotechnology, SASTRA University, Tirumalaisamudram, Thanjavur, India.
Gunasekaran SharmilaSchool of Chemical and Biotechnology, SASTRA University, Tirumalaisamudram, Thanjavur, India.
Konda KumaraswamiDepartment of Clinical Pharmacology and Therapeutics, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad, India.
Rupam BorghainDepartment of Neurology, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad, India.
Rukmini MridulaDepartment of Neurology, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad, India.
Vijay Kumar KutalaDepartment of Clinical Pharmacology and Therapeutics, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad, India. vijaykutala@gmail.com.
Nizam's Institute of Medical Sciences · INSASTRA University · INJawaharlal Nehru Technological University, Hyderabad · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a multi-factorial disorder with high-penetrant mutations accounting for small percentage of PD. Our previous studies demonstrated individual association of genetic variants in folate, xenobiotic, and dopamine metabolic pathways with PD risk. The rational of the study was to develop a risk prediction model for PD using these genetic polymorphisms along with synuclein (SNCA) polymorphism. We have generated additive, multifactor dimensionality reduction (MDR), recursive partitioning (RP), and artificial neural network (ANN) models using 21 SNPs as inputs and disease outcome as output. The clinical utility of all these models was assessed by plotting receiver operating characteristics curves where in area under the curve (AUC) was used as an index of diagnostic utility of the model. The additive model was the simplest and exhibited an AUC of 0.72. The MDR model showed significant gene-gene interactions between SNCA, DRD4VNTR, and DRD2A polymorphisms. The RP model showed SHMT C1420T as important determinant of PD risk. This variant allele was found to be protective and this protection was nullified by MTRR A66G. Inheritance of SHMT wild allele and SNCA intronic polymorphism was shown to increase the risk of PD. The ANN model showed higher diagnostic utility (AUC = 0.86) compared to all the models and was able to explain 56.6% cases of sporadic PD. To conclude, the ANN model developed using SNPs in folate, xenobiotic, and dopamine pathways along with SNCA has higher clinical utility in predicting PD risk compared to other models.

Indexed as

Models, GeneticAdultCase-Control StudiesFemaleHumansMaleMiddle AgedNeural Networks, ComputerParkinson DiseasePolymorphism, Single NucleotideArtificial neural networkDopamine pathwayFolate pathwayParkinson’s diseaseSynucleinXenobiotic pathway

Identifiers

PMID26438087
OpenAlexW1823874002

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Registered trials

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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.