Topic: astrocyte reactivity

Glioblastoma multiforme is the most common and aggressive malignant brain tumor in adults. One of the factors contributing to the progression is the complex tumor microenvironment. Specially, the coexistence of two cell types, tumoral cells and resident astrocytes, sharing genetic and phenotypical backgrounds. This aspect hinders the phenotypical and functional distinction of both cell types during tumor development. Here, we found a differential expression of the astrocytic markers GFAP and S100β that allowed us to histologically distinguish between tumoral cells and resident astrocytes in GB

Autism spectrum disorder (ASD) affects approximately 1 in 36 individuals, imposing lifelong challenges on patients. Yet still, effective treatments for ASD remain elusive. Rare mutations in the SETD5 (SET Domain Containing 5) gene, a chromatin regulator, have been firmly linked to ASD with high confidence. To date, reports studying the molecular role of SETD5 are limited and how exactly SETD5 haploinsufficiency leads to ASD remains unclear. Setd5-haploinsufficient mice have successfully demonstrated ASD-like behaviours, yet they fail to accurately replicate human brain development and patholog

Following injury, astrocytes undergo major alterations in morphology and gene expression, leading to the acquisition of distinct “reactivity” states that play important roles in brain tissue repair. Evidence indicates that these cellular states are also marked by rewiring of mitochondrial energy metabolism, i.e. the central hub for cellular energy metabolism and metabolic signaling. However, how such mitochondrial responses are regulated and how they may influence astrocyte reactivity remains unclear. Our prior research unveiled temporal and region-specific morphological changes in astrocytic