Juan Zhang and al.

In this study, the authors used a Tet-On 3G genetic approach to achieve precise temporal control of protein translation in the infralimbic (IL) medial prefrontal cortex of mice submitted a fear extinction model. The results reveal that Cpeb1 disruption during the fear extinction phase leads to significant changes in cell-type-specific translation programs, thereby affecting fear extinction. Specifically, neuronal KO of Cpeb1 activates the translation of the heterochromatin protein Hp1bp3, which enhances microRNA networks, while microglial Cpeb1 KO suppresses the translation of Cx3cr1, resulting in a microglial phenotype resembling that of aged microglia. The coordinated alterations induced by Cpeb1 KO prevent the synaptic remodeling events required for fear extinction.

Payam Gharibani and al.

In this study, the authors demonstrate that the protein kinase C (PKC) modulator, bryostatin-1 (bryo-1), induces the transition of microglia/macrophage from pro-inflammatory phenotypes to regenerative ones. These results are observed both in vitro and in vivo in the EAE model. Furthermore, systemic treatment of mice with bryo-1 stimulates remyelination following a focal demyelinating lesion.

Mary O’Keeffe and al.

The authors showed that several neurodevelopmental processes previously described as microglia-dependent can occur in the absence of microglia. Thus, in Csf1r∆FIRE/∆FIRE mice, which lack microglia, the authors reported that the number and maturation of synapses are normal in the CA1 region of the hippocampus as well as in the somatosensory cortex. Susceptibility to epileptic seizures is also normal in these mice. Finally, single-cell RNA-seq transcriptomic analyses did not reveal any substantial neuronal or astrocytic disturbances in the absence of microglia.

Claudia Cantoni and al.

In this study, a single-cell RNA-seq analysis was performed on cerebrospinal fluid (CSF) cells to elucidate the pathophysiology of various neurological diseases, including multiple sclerosis (MS), Alzheimer’s disease, Parkinson’s disease, COVID-19, and autoimmune encephalitis. The authors notably identified a novel subpopulation of CSF-specific dendritic cells expressing the gene AREG and being more abundant in individuals with MS compared to healthy controls.

Maïlis Darmuzey and al.

The authors of this study compared the neuropathogenicity of Zika virus (ZIKV) strains from Asia, isolated before and after the 2015-2016 outbreak. In murine prenatal models, all studied Asian ZIKV strains were neurovirulent, but the pre-outbreak strains were consistently more pathogenic than their epidemic counterparts. Pathogenicity was not directly related to viral replication. All ZIKV strains tested triggered an immune response, but epidemic strains induced a more attenuated immune response compared to pre-outbreak strains. These results demonstrate that Asian ZIKV strains have evolved towards attenuation of pathogenicity, which could explain the emergence of neonatal pathogenicity rather than premature death in utero.