Browse Articles

After spinal cord injury, stromal fibroblasts originate from pericytes and perivascular fibroblasts, with pericytes more prevalent in gray matter and fibroblasts in white matter. Holl et al. show that both cell types respond to injury and inflammation, are activated, and transcriptionally converge on scar formation after injury, paving the way for therapeutic possibilities.

Rational planning requires time spent thinking. Here, the authors propose a model of planning where a frontal network triggers hippocampal replay, integrating the replayed trajectory in its recurrent dynamics to improve decisions.

The origin and composition of stromal fibroblasts in the fibrotic CNS scar are unclear. Here, the authors demonstrate that pericytes and perivascular fibroblasts contribute to fibrotic scarring following spinal cord injury in mice in a region-dependent manner.

Here the authors show that ventrally derived oligodendrocytes (OLs) can myelinate areas usually populated by dorsally derived OLs but cannot functionally compensate, as animals populated only by ventrally derived OLs show locomotor and cognitive deficits.

Cognitive control is important for later-life success and is often targeted for interventions. Here the authors show that response inhibition training in a large sample of children over 8 weeks did not change their brains or behavior in the short or long term.

Specifically mutating the neurofibromatosis type 1 gene (NF1) in oligodendrocyte precursor cells (OPCs) impairs their adaptive response to neuronal activity and their differentiation into mature oligodendrocytes, as well as promoting focal regions of OPC hyperdensity. These defects delay oligodendroglial development and impede adaptive oligodendrogenesis, which are important for motor learning.

BrainTF is the largest study to date that directly measures transcription factor (TF) binding in human postmortem brain, demonstrating improved measurements of TF activity and nominating TFs whose occupancy is enriched for risk variants of neuropsychiatric disorders.

Activity-dependent oligodendroglial plasticity contributes to neuronal functions. Here the authors show that adaptive oligodendrocyte progenitor cell responses are disrupted in neurofibromatosis 1, impairing oligodendroglial dynamics and resulting in motor learning deficits in Nf1-deficient and Nf1-mutant mice.

The axon guidance receptor Plexin-B1 regulates the cellular interaction of peri-plaque astrocytes with microglia to affect the pathophysiology of Alzheimer’s disease.

Oligodendrocyte-lineage NG2 glia are shown to limit prion-induced neurodegeneration by quenching toxic microglial responses. Their depletion unleashes prostaglandin E2 secretion by microglia and contributes non-cell-autonomously to prion toxicity.

Intersectional adeno-associated viruses are important for neuroscience research but can be limited by complex and bulky design parameters. Hughes et al. present a unique and space-saving approach that simplifies toolkit development and provides expanded functionality.

This paper presents Simple Behavioral Analysis (SimBA), an open-source platform for automated, explainable machine learning analysis of behavior. SimBA comes with extensive documentation, a graphical interface and an active community and works with any organism tracked by pose estimation.

How the brain tracks blood glucose dynamics is unclear. Viskaitis et al. show that hypothalamic orexin/hypocretin cells track glucose concentration and rate of change and that their activity is important for glucose-evoked locomotor suppression.

LINE-1 retrotransposons are a type of mobile DNA element normally repressed in the body. Here the authors show that LINE-1 sequences can jump in mouse parvalbumin interneurons and also promote the transcription of key parvalbumin interneuron genes.

Mature myelin has been considered static, though recent evidence indicates it is in fact dynamic. Here, Osso and Hughes review the dynamics of mature myelin, a form of neuroplasticity, from myelin turnover to remodeling of myelin structure. The authors consider the mechanisms that regulate these dynamics and the functional implications of mature myelin remodeling.

By using genetic admixture in the multi-omic analysis of postmortem brains from Black Americans, we show that genetic ancestry influences gene expression in the brain. Notably, we find enrichment of ancestry-associated genes for immune response and vascular function, but not neuronal function. Our findings have potential implications for stroke, Parkinson’s disease and Alzheimer’s disease.

The increased inclusion of samples from individuals from minoritized communities in biomedical research will help to mitigate health disparities that stem from a medical enterprise founded in racism and exclusion. In this issue of Nature Neuroscience, Benjamin et al. investigate how genetic ancestry influences the expression of genes in the brain, an effort supported by community leaders who raised funding, partnered in shaping research questions and had a central role in the interpretation and communication of the study’s findings. Here, we outline the public and social context that motivated these efforts towards ensuring equitable access to the benefits of science for all.

Studying gene expression in admixed Black Americans, Benjamin et al. reveal genetic ancestry-linked differences impacting immune and vascular genes and potentially influencing neurological disease risk. These findings highlight the importance of considering ancestry in brain research.

The circuit mechanisms underlying emotion recognition are unclear. Here, Dautan et al. show a role for a long-range feedback loop comprising somatostatin inhibitory projections from the medial prefrontal cortex (mPFC) to the retrosplenial cortex (RSC) and excitatory feedback projections from the RSC to the mPFC.