News & Views

Disrupting reconsolidation of the maladaptive memories underlying post-traumatic stress disorder (PTSD) could be transformative for treatment. However, patients cannot undergo the direct re-exposure to trauma-cues used to induce reconsolidation in animal studies. Ressler and colleagues report ‘covert’ memory reactivation in rats, bolstering hopes for translation of reconsolidation-based interventions.

Dong and colleagues investigated mechanisms mediating neurodegeneration in multiple sclerosis and identified a direct role for oxidized phosphatidylcholines (OxPCs) in driving CNS cell death. Microglia activity, mediated by the lipid sensor TREM2 and a neutralizing OxPC antibody, were capable of rescuing OxPC-induced neurotoxicity.

How does the intricate balance of gene regulation and expression within individual neurons relate to electrophysiological oscillations and, ultimately, cognition? In a new study, Berto and colleagues take an important step toward addressing this question by correlating oscillatory biomarkers of successful memory encoding with gene expression on a within-participant basis.

Persistent negative emotional states, such as anxiety, suppress social behavior and vice versa. A new report identifies a novel neural circuit that generates persistent anxiety states and describes how competing excitatory and inhibitory components of this circuit battle to pattern social behavior.

By probing the dependence on learning history or motivational significance of stimuli, Sharpe and colleagues reveal previously uncharacterized contributions of lateral hypothalamus GABA neurons to associative learning.

A new study discovered that ventral pallidal neurons projecting back to the nucleus accumbens promote consumption. The findings call into question the accepted direction of information flow through the ventral basal ganglia and open new avenues for studying how consumption is regulated in proportion to subjective value.

Fibrotic scarring after inflammation is well-characterized in peripheral tissues, but its role in the CNS is less clear. A new study shows that local proliferation of CNS fibroblasts drives fibrotic scar formation in response to circulating inflammatory cell infiltration in a model of multiple sclerosis, which may limit repair.

A new study reveals that maternal immune activation promotes sex-biased activation of the integrated stress response in the developing mouse brain and that this mechanistically contributes to the onset of autism-related behaviors uniquely in male offspring.

A new study proposes an exciting new model of neuronal diversification in the developing enteric nervous system (ENS) and establishes a detailed molecular taxonomy for enteric neurons. Their findings open new horizons for ENS research and for developing cell-based therapies for ENS disorders.

One of the mechanisms driving aging and neurodegenerative diseases is the accumulation of senescent cells, while their elimination mitigates age-related decline. A new report details how, with aging, changes in the dentate gyrus microenvironment lead to natural-killer-cell-mediated clearance of neurogenic senescent cells, resulting in cognitive decline.

Network neuroscientists envision the brain as a network of nodes (regions) linked via edges (connections). A long-held assumption is that node-centric interactions are the primary phenomena of interest. Faskowitz et al. introduce a novel edge-centric framework with the potential to usher in a new era of discovery in connectomics research.

Chiot and colleagues investigated whether peripheral macrophages play a role in amyotrophic lateral sclerosis (ALS) pathology, finding that macrophages along peripheral motor neuron axons react to neurodegeneration. Modifying reactive oxygen species (ROS) signaling in peripheral macrophages, using bone marrow cell replacement, reduces both macrophage and microglia inflammatory response, delays pathology and increases survival in ALS mouse models.

By building a richer behavioral vocabulary, Wiltschko et al. tease apart subtle differences in how pharmacological agents affect animal behavior, mapping on- and off-target effects of drugs with improved precision.

Abrupt spatial changes in anatomic and functional properties of the brain demarcate boundaries between discrete functional areas. While previous work has identified these boundaries in cortex, a new study by Tian et al. applies this approach for the first time to subcortical structures within the in vivo human brain.

A new study shows that, immediately after axon injury, glycolysis is increased in Schwann cells to provide axons with energy and prevent them from degenerating. The authors also identify possible therapeutic targets that could be modulated to promote axonal protection.

Sleep is controlled by a cocktail of neurotransmitters, but it is difficult to measure these in the brain. A new study by Tamaki et al. reveals how the balance between excitation and inhibition oscillates as the brain moves through sleep stages and how this impacts upon memory consolidation and stabilization.

Pathological tau disrupts the association between nitric oxide (NO) synthase and PSD95, impairing NO signaling and neurovascular coupling before causing neurodegeneration. Stopping production of pathological tau rescues NO signaling, neurovascular coupling and neuronal function, but doesn’t remove tangles, suggesting that (like amyloid-β) soluble tau is an important driver of early neurovascular dysfunction and subsequent neuronal damage.

A new technique developed by Garcia-Marques and colleagues uses CRISPR–Cas9 editing to activate an ordered sequence of fluorescent markers in stem cells and their progeny. These tools represent a new way to probe the spatial and temporal patterns of cell lineage progression.

Following learning, memories for events are reorganized in a time-dependent manner in distributed hippocampal–cortical networks. While previous studies have focused on neural contributions to this process of systems consolidation, a new study by Kol et al. reveals that astrocytes play crucial modulatory roles in the formation of remote memories.

Poll and colleagues examined the historical activity of hippocampal CA1 neurons during learning and memory recall using longitudinal two-photon in vivo imaging, providing evidence that extra neural ensemble activity disrupts memory recall in a mouse model of early Alzheimer’s disease.