Yuan et al. find that the kidney can serve as a site of initiation for the spread of pathological α-synuclein to the brain, contributing to the development of Parkinson’s disease (PD) and providing a mechanistic link between PD and renal dysfunction.

The authors show that a bidirectional circuit connecting the anterior and posterior (aIC–pIC) insula mediates the conditioned immune response in male mice, illustrating a mechanism by which sensory experience affects immune function.

The default mode network (DMN) is implicated in cognition and behavior. Here, the authors show that the DMN is cytoarchitecturally heterogeneous, it contains regions receptive to input from the sensory cortex and a core relatively insulated from environmental input, and it uniquely balances its output across sensory hierarchies.

Using a novel method for isolating cognitive and motor neural dynamics, the authors show that dynamics often attributed to cognitive processes were corrupted by movements and that distinct populations of neurons encode cognitive and motor variables.

The authors show that brain inflammation in COVID-19 correlates with viral load, systemic inflammation and virus-sensing pattern recognition receptors. Microglial dysfunction occurs at sites of vascular inflammation with myelin injury and synapse loss.

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.

A founding father of neuroscience.