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Format should be in the following format: Activity Code, Institute Abbreviation, and Serial Number. Grant Type, Support Year, and Suffix should be excluded. For example, grant 1R01MH123456-01A1 should be entered R01MH123456

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SelectExperiment IdExperiment NameExperiment Type
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  • EEG
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Created On
886RestfMRI02/14/2018
885SARTfMRI02/14/2018
884Plasma metabolic profileOmics02/05/2018
878Social Challenge AssessmentEye Tracking01/26/2018
877PRV-005-EEGEEG01/22/2018
876Mixed Anti and Pro (vgs) saccade mixed blocked eye trackingEye Tracking01/22/2018
875Attention modulation taskEye Tracking01/17/2018
874ruthldopa resting 17 and 18fMRI01/16/2018
873ruthldopa resting 15 and 16fMRI01/16/2018
872ruthldopa resting 13 and 14fMRI01/16/2018
871ruthldopa resting 11 and 12fMRI01/16/2018
870Resting State fMRIfMRI01/12/2018
869cyberballfMRI01/12/2018
868MDD_PilotfMRI01/12/2018
867Velten Mood Induction State-ItemfMRI01/12/2018
866Emotional Hemifield Task (EHT)EEG01/12/2018
865Genome EditingOmics01/12/2018
864parvizi_eeg_118EEG01/12/2018
863parvizi_eeg_117EEG01/12/2018
862parvizi_eeg_116EEG01/12/2018
861parvizi_eeg_115EEG01/12/2018
860parvizi_eeg_114EEG01/12/2018
859parvizi_eeg_113EEG01/12/2018
858PRV-003-EEGEEG01/12/2018
857PRV-004-EEGEEG01/12/2018
856PRV-007-EEGEEG01/12/2018
855Regulating Emotional Responses to Visual Images Across the Affective Instability SpectrumfMRI01/12/2018
854PRV-002-EEGEEG01/12/2018
853R61 Ezogabine Resting State FMRIfMRI01/11/2018
852Paired AssociatesfMRI01/11/2018
851PRV-001-EEGEEG01/11/2018
850Reward ProcessingfMRI01/11/2018
849Resting EEG (1024 samples/s)EEG01/11/2018
845Fast face -1 runfMRI01/10/2018
844MIST_MAST_fMRIfMRI01/10/2018
843RTT AHA-1Omics01/09/2018
84230 words (simultaneous fMRI and EEG acquisition)EEG01/08/2018
841Neural Correlates of Episodic Retrieval fMRI01/08/2018
84030 words (simultaneous fMRI and EEG acquisition)fMRI01/08/2018
838Memory Guided Saccade Encode and Maintenance v3fMRI01/05/2018
837Memory Guided Saccade Encode and Maintenance v2fMRI01/05/2018
836Food ExposurefMRI01/03/2018
835Model ExposurefMRI01/02/2018
834BlankingEye Tracking12/28/2017
833DoubleStepEye Tracking12/26/2017
832Memory Guided Saccade Encode and Maintenance v1 fMRI12/21/2017
831Mixed Anti and Pro (vgs) saccade mixed blocked taskfMRI12/21/2017
830T1 AlternativefMRI12/19/2017
829fMRI Movie Trailer Video 2fMRI12/18/2017
828fMRI Movie Trailer Video 1fMRI12/18/2017
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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
Funding Completed
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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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Experiments

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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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Shared Data

Data structures with the number of subjects submitted and shared are provided.

Genomics Sample Genomics 100
Genomics Subject Genomics 100

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Publications

Publications relevant to NDAR data are listed below. Most displayed publications have been associated with the grant within Pubmed. Use the "+ New Publication" button to add new publications. Publications relevant/not relevant to data expected are categorized. Relevant publications are then linked to the underlying data by selecting the Create Study link. Study provides the ability to define cohorts, assign subjects, define outcome measures and lists the study type, data analysis and results. Analyzed data and results are expected in this way.

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
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genomics/omics info iconApproved
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Associated Studies

Studies that have been defined using data from a Collection are important criteria to determine the value of data shared. The number of subjects column displays the counts from this Collection that are included in a Study, out of the total number of subjects in that study. The Data Use column represents whether or not the study is a primary analysis of the data or a secondary analysis. State indicates whether the study is private or shared with the research community.

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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