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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 NeuroBioBankFeatured Publication
ATM-deficiency-induced microglial activation promotes neurodegeneration in ataxia-telangiectasia.
While ATM loss of function has long been identified as the genetic cause of ataxia-telangiectasia (A-T), how it leads to selective and progressive degeneration of cerebellar Purkinje and granule neurons remains unclear. ATM expression is enriched in…
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Hedonic eating, obesity, and addiction result from increased neuropeptide Y in the nucleus accumbens during human brain evolution.
The nucleus accumbens (NAc) is central to motivation and action, exhibiting one of the highest densities of neuropeptide Y (NPY) in the brain. Within the NAc, NPY plays a role in reward and is involved in emotional behavior and in increasing alcohol…
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Heart failure-induced cognitive dysfunction is mediated by intracellular Ca<sup>2+</sup> leak through ryanodine receptor type 2.
Cognitive dysfunction (CD) in heart failure (HF) adversely affects treatment compliance and quality of life. Although ryanodine receptor type 2 (RyR2) has been linked to cardiac muscle dysfunction, its role in CD in HF remains unclear. Here, we show…
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