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The link between neuroinflammation and the progression of multiple sclerosis (MS) is unclear. Here, the authors show that in MS lesions, neuronal somatic mutations accumulate 2.5 times faster than in controls, equivalent to 1,291 excess mutations by age 70, suggesting that neuroinflammation can be mutagenic.
The mechanisms of pathological astrocyte responses during multiple sclerosis remain unclear. Kadowaki et al. found in MS mouse models that CLEC16A suppresses astrocyte pathogenic activities related to mitochondria by boosting mitophagy.
The role of lateral inhibition for perception and neural computation remains unsolved. Del Rosario et al. show that distinct types of cortical interneurons in V1 drive lateral inhibition that causes subtraction or division of visual sensitivity.
Nasal anti-CD3 therapy shows promise for treating traumatic brain injury by reducing neuroinflammation and aiding recovery in mice. It induces interleukin-10-producing regulatory T cells that enhance microglial phagocytic activity and reduce chronic inflammation, potentially aiding brain repair.
The mechanisms of neurovascular adaptations underlying stress resilience remain unclear. Here the authors show that the astrocytic endocannabinoid system modulates the blood–brain barrier changes during stress in adult mice.
Changes in blood–brain barrier (BBB) properties and endocannabinoid system function contribute to stress responses and have been implicated in the development of mood disorders. Here, we report a mechanism linking both systems, in which neurovascular endocannabinoids prevented loss of BBB integrity induced by stress-related inflammation, resulting in stress resilience.
Lipidomics revealed that neurons of patients with ALS/FTD have reduced levels of polyunsaturated fatty acid (PUFA)-containing phospholipids. Increasing neuronal PUFA levels increased survival of Drosophila models of ALS/FTD and patient neurons, suggesting that interventions that increase neuronal PUFA levels in patients with ALS/FTD may also be beneficial.
The authors show PTEN mutations, which can cause both congenital hydrocephalus and autism spectrum disorder, disrupt CSF homeostasis and brain connectivity in mice. Reducing mTORC1 activation ameliorates ventricular enlargement and neuronal deficits.
Socioeconomic status is multidimensional and can change over time. Xu, Lui, Ji et al. found dimension-specific, late-stage-specific and change-specific socioeconomic effects on brain, cognition, personality and emotion.
White matter (WM) astrocytes differ significantly from gray matter astrocytes, with WM astrocytes in the forebrain exhibiting unique proliferation capacity, which is absent in cerebellar WM, suggesting region-specific astrocyte generation.
Through circuit dissection in juvenile, adolescent and adult mice, Klune, Goodpaster and colleagues reveal multiple developmental switches in mPFC–NAc and mPFC–BLA pathways that underlie developmental transitions in threat avoidance behavior.
Distinct hippocampal feedback pathways to deep and superficial layers of the cortex in mice differentially modulate excitation–inhibition dynamics, plasticity and cognitive behavioral output.
Bernier, Hefendehl et al. describe a stromal progenitor cell population consisting of pericytes, venular smooth muscle cells and perivascular fibroblasts in the adult brain that modify their function and coordinate blood vessel repair following stroke.
Sehgal et al. show that branch-specific dendritic plasticity mechanisms in the retrosplenial cortex link memories acquired close in time such that, unlike independent memories, linked memories are encoded by many of the same dendritic branches.
The latent circuit model identifies low-dimensional mechanisms of task execution from heterogenous neural responses. This approach reveals a latent inhibitory mechanism for context-dependent decisions in neural network models and the prefrontal cortex.
Animals must distinguish between signals from sensory stimuli and action-generated signals. This paper shows that the ventral lateral geniculate nucleus acts as a corollary discharge center to suppress motion-induced visual signals, orchestrating accurate perception and motor control.
