Scientific Researchers
Learn how to request tissue from the NeuroBioBank or browse our inventory of available samples.
Potential Donors
Learn about the crucial need for brain donation and how your gift can advance human knowledge.
Because of a lapse in government funding, the information on this website may not be up to date, transactions submitted via the website may not be processed, and the agency may not be able to respond to inquiries until appropriations are enacted. The NIH Clinical Center (the research hospital of NIH) is open. For more details about its operating status, please visit cc.nih.gov. Updates regarding government operating status and resumption of normal operations can be found at OPM.gov.
This repository is under review for potential modification in compliance with Administration directives.
Since 2013, the NIH NeuroBioBank has catalyzed scientific discovery through the centralization of resources aimed at the collection and distribution of human post-mortem brain tissue.
Our networked brain and tissue repositories distribute thousands of samples per year to the research community studying neurological, developmental, and psychiatric disorders.
Learn more about the NIH NeuroBioBankLearn how to request tissue from the NeuroBioBank or browse our inventory of available samples.
Learn about the crucial need for brain donation and how your gift can advance human knowledge.
Analysis of microisolated frontal cortex excitatory layer III and V pyramidal neurons reveals a neurodegenerative phenotype in individuals with Down syndrome.
We elucidated the molecular fingerprint of vulnerable excitatory neurons within select cortical lamina of individuals with Down syndrome (DS) for mechanistic understanding and therapeutic potential that also informs Alzheimer's disease (AD) pathophy…
View the abstractDNA mismatch and damage patterns revealed by single-molecule sequencing.
Mutations accumulate in the genome of every cell of the body throughout life, causing cancer and other diseases1,2. Most mutations begin as nucleotide mismatches or damage in one of the two strands of the DNA before becoming double-strand…
View the abstractMis-spliced transcripts generate <i>de novo</i> proteins in TDP-43-related ALS/FTD.
Functional loss of TDP-43, an RNA-binding protein genetically and pathologically linked to ALS and FTD, leads to inclusion of cryptic exons in hundreds of transcripts during disease. Cryptic exons can promote degradation of affected transcripts, del…
View the abstract