Continuing trial responsibilities for implantable neural devices.

Participants of neural implant studies have research-related posttrial care needs (e.g., hardware replacements).

Advancing scientific excellence through inclusivity in the NIH BRAIN Initiative.

Leveraging breadth and depth of the scientific workforce invites creativity, relevance, and differing views that directly tie into innovation and problem solving. The NIH BRAIN Initiative is using a multi-pronged strategy to enhance diversity and inclusion toward promoting the best science.

A call to action to address rural mental health disparities.

Rural residents in the USA experience significant disparities in mental health outcomes even though the prevalence of mental illness in rural and metropolitan areas is similar. This is a persistent problem that requires innovative approaches to resolve. Adopting and appropriately modifying the National Institute on Minority Health and Health Disparities research framework are the potential approaches to understanding how these disparities might be addressed through research.

Alaska Native genomic research: perspectives from Alaska Native leaders, federal staff, and biomedical researchers.

Meaningful engagement of Alaska Native (AN) tribes and tribal health organizations is essential in the conduct of socially responsible and ethical research. As genomics becomes increasingly important to advancements in medicine, there is a risk that populations not meaningfully included in genomic research will not benefit from the outcomes of that research. AN people have historically been underrepresented in biomedical research; AN underrepresentation in genomics research is compounded by mistrust based on past abuses, concerns about privacy and data ownership, and cultural considerations specific to this type of research.

Accelerating a paradigm shift: The Common Fund Single Cell Analysis Program.

It has become exceedingly important to understand the precise molecular profiles of the nearly 40 trillion cells in an adult human because of their role in determining health, disease, and therapeutic outcome. The National Institutes of Health (NIH) Common Fund-supported Single Cell Analysis Program (SCAP) was designed to address this challenge. In this review, we outline the original program goals and provide a perspective on the impact of the program as a catalyst for exploration of heterogeneity of human tissues at the cellular level.

Epigenetics in the nervous system.

It is becoming increasingly clear that epigenetic modifications are critical factors in the regulation of gene expression. With regard to the nervous system, epigenetic alterations play a role in a diverse set of processes and have been implicated in a variety of disorders. Gaining a more complete understanding of the essential components and underlying mechanisms involved in epigenetic regulation could lead to novel treatments for a number of neurological and psychiatric conditions.

Corticosterone response to acute stress in a mouse model of Fragile X syndrome.

Fragile X syndrome (FXS), the most common form of inherited mental retardation, results from the silencing of the Fmr1 gene that encodes the Fragile X mental retardation protein (FMRP). Because (1) mRNA for the glucocorticoid receptor is bound by FMRP and (2) the response to acute stress is elevated in children with FXS, we examined whether this heightened response is characteristic of a mouse model of FXS. Fmr1 knockout (KO) and wildtype (WT) control mice were exposed to 30 min of acute restraint; serum corticosterone levels were assayed from unstressed animals and those examined either immediately following stress or after a 15 or 60 min recovery period.

Poly(A) tail length-dependent stabilization of GAP-43 mRNA by the RNA-binding protein HuD.

The neuronal ELAV-like RNA-binding protein HuD binds to a regulatory element in the 3'-untranslated region of the growth-associated protein-43 (GAP-43) mRNA. Here we report that overexpression of HuD protein in PC12 cells stabilizes the GAP-43 mRNA by delaying the onset of mRNA degradation and that this process depends on the size of the poly(A) tail. Using a polysome-based in vitro mRNA decay assay, we found that addition of recombinant HuD protein to the system increased the half-life of full-length, capped, and polyadenylated GAP-43 mRNA and that this effect was caused in part by a decrease in the rate of deadenylation of the mRNA.