Brain Tissue Collection for Neuropathological Studies
Brain Procurement for the Human Brain Collection Core
2 other identifiers
observational
2,161
1 country
3
Brief Summary
The purpose of this study is to collect and study the brain tissue of deceased individuals to learn more about the nervous system and mental disorders. Information gained from donated tissue may lead to better treatments and potential cures for nervous system and mental disorders. This study will ask relatives of deceased individuals to donate the brains of their deceased relatives to allow further study of neurological and psychiatric disorders. We do not accept prospective donations.
Trial Health
Trial Health Score
Automated assessment based on enrollment pace, timeline, and geographic reach
participants targeted
Target at P75+ for all trials
Started May 1990
Longer than P75 for all trials
3 active sites
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
Click on a node to explore related trials.
Study Timeline
Key milestones and dates
Study Start
First participant enrolled
May 29, 1990
CompletedFirst Submitted
Initial submission to the registry
November 3, 1999
CompletedFirst Posted
Study publicly available on registry
November 4, 1999
CompletedStudy Completion
Last participant's last visit for all outcomes
June 16, 2017
CompletedDecember 9, 2019
June 16, 2017
November 3, 1999
December 6, 2019
Conditions
Keywords
Eligibility Criteria
You may qualify if:
- Brain tissue is needed from individuals suffering from a variety of neuropsychiatric disorders, especially schizophrenia, but also anxiety disorders, suicide, bipolar disorder, depression, Tourette's Syndrome, drug addictions (PCP, cocaine, alcohol, heroin or the like) and any form of dementia. In addition, brains from normal individuals without a history of neuropsychiatric disease will be needed for controls.
You may not qualify if:
- No living subjects are enrolled in this protocol. Tissue is obtained after death, with the permission of next of kin, or from existing institutions with appropriate samples via an MTA or other applicable agreement.
- Brain tissue is excluded from collection if there is a previously known history of strokes, lesions, or other major neuropathological abnormalities prior to the consenting process.
Contact the study team to confirm eligibility.
Sponsors & Collaborators
Study Sites (3)
Office of the Chief Medical Examiner
Washington D.C., District of Columbia, 20003, United States
National Institutes of Health Clinical Center, 9000 Rockville Pike
Bethesda, Maryland, 20892, United States
Office of the Chief Medical Examiner
Fairfax, Virginia, 22032, United States
Related Publications (7)
Meyer-Lindenberg A, Straub RE, Lipska BK, Verchinski BA, Goldberg T, Callicott JH, Egan MF, Huffaker SS, Mattay VS, Kolachana B, Kleinman JE, Weinberger DR. Genetic evidence implicating DARPP-32 in human frontostriatal structure, function, and cognition. J Clin Invest. 2007 Mar;117(3):672-82. doi: 10.1172/JCI30413. Epub 2007 Feb 8.
PMID: 17290303BACKGROUNDLaw AJ, Lipska BK, Weickert CS, Hyde TM, Straub RE, Hashimoto R, Harrison PJ, Kleinman JE, Weinberger DR. Neuregulin 1 transcripts are differentially expressed in schizophrenia and regulated by 5' SNPs associated with the disease. Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6747-52. doi: 10.1073/pnas.0602002103. Epub 2006 Apr 17.
PMID: 16618933BACKGROUNDEgan MF, Straub RE, Goldberg TE, Yakub I, Callicott JH, Hariri AR, Mattay VS, Bertolino A, Hyde TM, Shannon-Weickert C, Akil M, Crook J, Vakkalanka RK, Balkissoon R, Gibbs RA, Kleinman JE, Weinberger DR. Variation in GRM3 affects cognition, prefrontal glutamate, and risk for schizophrenia. Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12604-9. doi: 10.1073/pnas.0405077101. Epub 2004 Aug 13.
PMID: 15310849BACKGROUNDBowen EFW, Burgess JL, Granger R, Kleinman JE, Rhodes CH. DLPFC transcriptome defines two molecular subtypes of schizophrenia. Transl Psychiatry. 2019 May 9;9(1):147. doi: 10.1038/s41398-019-0472-z.
PMID: 31073119DERIVEDMansur RB, Fries GR, Trevizol AP, Subramaniapillai M, Lovshin J, Lin K, Vinberg M, Ho RC, Brietzke E, McIntyre RS. The effect of body mass index on glucagon-like peptide receptor gene expression in the post mortem brain from individuals with mood and psychotic disorders. Eur Neuropsychopharmacol. 2019 Jan;29(1):137-146. doi: 10.1016/j.euroneuro.2018.10.007. Epub 2018 Nov 6.
PMID: 30409537DERIVEDMansur RB, Fries GR, Subramaniapillai M, Frangou S, De Felice FG, Rasgon N, McEwen B, Brietzke E, McIntyre RS. Expression of dopamine signaling genes in the post-mortem brain of individuals with mental illnesses is moderated by body mass index and mediated by insulin signaling genes. J Psychiatr Res. 2018 Dec;107:128-135. doi: 10.1016/j.jpsychires.2018.10.020. Epub 2018 Oct 27.
PMID: 30391805DERIVEDXiao X, Zhang C, Grigoroiu-Serbanescu M, Wang L, Li L, Zhou D, Yuan TF, Wang C, Chang H, Wu Y, Li Y, Wu DD, Yao YG, Li M. The cAMP responsive element-binding (CREB)-1 gene increases risk of major psychiatric disorders. Mol Psychiatry. 2018 Sep;23(9):1957-1967. doi: 10.1038/mp.2017.243. Epub 2017 Nov 21.
PMID: 29158582DERIVED
MeSH Terms
Conditions
Condition Hierarchy (Ancestors)
Study Officials
- PRINCIPAL INVESTIGATOR
Jose A Apud, M.D.
National Institute of Mental Health (NIMH)
Study Design
- Study Type
- observational
- Sponsor Type
- NIH
- Responsible Party
- SPONSOR
Study Record Dates
First Submitted
November 3, 1999
First Posted
November 4, 1999
Study Start
May 29, 1990
Study Completion
June 16, 2017
Last Updated
December 9, 2019
Record last verified: 2017-06-16