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Collection Summary Collection Charts
Collection Title Collection Investigators Collection Description
Reduced NADH Production in the Presence of Tryptophan as a Biomarker of ASD
Charles Schwartz 
Autism Spectrum Disorders (ASDs) affect 1/110 children in the United States, but physicians do not yethave an effective laboratory test which can confirm the clinical diagnosis. This proposal aims to develop aquick and reliable metabolic array to identify individuals with ASD.Using Phenotype Microarray plates obtained from Biolog (Hayward, CA), we have been able to showthat Nicotinamide Adenine Dinucleotide, reduced form (NADH) production in the presence of tryptophan asonly energy source in lymphoblastoid cells was consistently reduced in 54/56 (96.4%) patients with ASD whencompared to 40 controls.The first aim of the proposed project is to validate our preliminary findings using a cohort of 50additional patients and 50 additional controls employing customized Phenotype Microarray plates. The newplates will allow us to test 12 individuals per plate, using just 160,000 cells per individual. The proposed 100samples, in addition to the 96 samples from the preliminary study, will give statistical power of 95.6% in a onesidedt-test at significance level of 0.01.The second aim is to use our assay to evaluate the NADH production in the presence of tryptophan infresh blood samples. As a first step, we plan to use 6 patients and 6 controls that we have already tested toreplicate the results observed in lymphoblastoid cell lines in fresh white cells. This first stage will allow us todetermine if we are able to observe the same low levels of NADH production in the presence of tryptophan inleukocytes as was observed in lymphoblasts. Next, we will test fresh blood samples from 12 patients with ASDand 12 controls. To reduce output variability, we will try to start the test at the same time for all the samples,coordinating the sampling of the 24 individuals. Finally, we will test 24 patient and 24 control blood samplesfrom new individuals in a blinded fashion to establish the predictive power of this test in patients with ASD. Forthis last part of the experiment, we will test each sample as soon as it arrives at our laboratory. We will use asingle row of 8 wells on the customized plates for each individual, covering the rest of the plate with aluminumfoil, to preserve the other rows for future tests.If our preliminary findings in lymphoblasts are confirmed in leukocytes, we would be able to develop areliable, easy to perform, inexpensive laboratory test which could provide a diagnosis in about 4-5 days. Sucha test could represent the first biochemical screening test for ASDs.
NDAR
Closed
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$269,884.00
100
84
11
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NIH - Extramural None


R21HD072473-01 Novel Metabolic Biomarker for Autism Spectrum Disorder 03/09/2012 02/28/2014 84 11 GREENWOOD GENETIC CENTER $269,884.00

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IDNameCreated DateStatusType
287Reduced NADH Production in the Presence of Tryptophan as a Biomarker of ASD04/02/2015ApprovedOmics

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Genomics Sample Genomics 100
Genomics Subject Genomics 100

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PubMed IDStudyTitleJournalAuthorsDateStatus
25559331Create StudyProtein sector analysis for the clustering of disease-associated mutations.BMC genomicsGuevara-Coto J, Schwartz CE, Wang L2014Not Determined
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Data Expected
Data ExpectedTargeted EnrollmentInitial SubmissionSubjects SharedStatus
Research Subject and Pedigree info iconApproved
genomics/omics info iconApproved
Structure not yet defined

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Associated Studies

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Study Name Description Number of Subjects
Collection / Total
Data Use State
Decreased tryptophan metabolism in patients with Autism Spectrum Disorders Background: Autism spectrum disorders (ASDs) are relatively common neurodevelopmental conditions whose biological basis has been incompletely determined. Several biochemical markers have been associated with ASDs, but there is still no laboratory test for these conditions. Methods: We analyzed the metabolic profile of lymphoblastoid cell lines from 137 patients with neurodevelopmental disorders with or without ASDs and 78 normal individuals, using Biolog Phenotype MicroArrays. Results: Metabolic profiling of lymphoblastoid cells revealed that the 87 patients with ASD as a clinical feature, as compared to the 78 controls, exhibited on average reduced generation of NADH when tryptophan was the sole energy source. The results correlated with the behavioral traits associated with either syndromal or non-syndromal autism, independent of the genetic background of the individual. The low level of NADH generation in the presence of tryptophan was not observed in cell lines from non-ASD patients with intellectual disability, schizophrenia or conditions exhibiting several similarities with syndromal autism except for the behavioral traits. Analysis of a previous small gene expression study found abnormal levels for some genes involved in tryptophan metabolic pathways in 10 patients. Conclusions: Tryptophan is a precursor of important compounds, such as serotonin, quinolinic acid, and kynurenic acid, which are involved in neurodevelopment and synaptogenesis. In addition, quinolinic acid is the structural precursor of NAD+, a critical energy carrier in mitochondria. Also, the serotonin branch of the tryptophan metabolic pathway generates NADH. Lastly, the levels of quinolinic and kynurenic acid are strongly influenced by the activity of the immune system. Therefore, decreased tryptophan metabolism may alter brain development, neuroimmune activity and mitochondrial function. Our finding of decreased tryptophan metabolism appears to provide a unifying biochemical basis for ASDs and perhaps an initial step in the development of a diagnostic assay for ASDs. Keywords: Autism, Biomarker, Tryptophan, Metabolism, Screening 100 / 100 Primary Analysis Shared
* Data not on individual level
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