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Microglia exhibit unexpected sex differences in gene expression and accessibility and compromised inflammatory responses during the aging process in mice. We established a mouse model with accelerated microglial turnover (3xDR), which results in aged microglia in non-aged brains. Analysis of this model revealed that aged microglia themselves contribute to cognitive decline.
Sa et al. identified a distinct neuronal subpopulation that controls brown adipose tissue thermogenesis. In mice fed a high-fat diet, hypothalamic GABRA5 neurons are deactivated by GABA released by surrounding astrocytes and inhibition of GABA synthesis ameliorates diet-induced obesity.
Human glial progenitors transplanted into a chimeric mouse brain replace sick or older human glia, a finding that could one day lead to new treatments for neurological disease.
The role of microglia in amyotrophic lateral sclerosis (ALS) is unclear. Here, the authors show that iPSC microglia from C9orf72-ALS patients are toxic to motor neurons and identify microglial MMP9 as a potential therapeutic target.
The role of lactate in the control of microglial function remains poorly investigated. Here, the authors show that lactate promotes lysosomal acidification in microglia, and that mice lacking the lactate transporter MCT4 in these cells display defective brain development and anxiety-like behavior.
Calcium dynamics and their role in oligodendrocyte precursor cells (OPCs) are unclear. In this study, the authors show that calcium dynamics at the processes of OPCs are modulated by norepinephrine and influence OPC proliferation during arousal in awake adult mice.
The transcriptional program underlying the origin of glial cells is unclear. Here the authors leverage single-cell/single-nucleus transcriptional and chromatin accessibility profiling to identify candidate cell fate specification genes and optimize a rapid astrocyte differentiation protocol.
Li et al. provide a transcriptional and epigenetic characterization of microglia in aging mice brain by developing a three-round depletion–repopulation (3xDR) model to study aged microglia in non-aged brain, giving insights into the molecular mechanism underlying microglia aging.
Increasing levels of glial-derived neurotrophic factor using a gene-therapy approach in a macaque model of alcohol use disorder resulted in a lower tendency to relapse into alcohol consumption after a period of abstinence.
Microglia exhibit unexpected sex differences in gene expression and accessibility and compromised inflammatory responses during the aging process in mice. We established a mouse model with accelerated microglial turnover (3xDR), which results in aged microglia in non-aged brains. Analysis of this model revealed that aged microglia themselves contribute to cognitive decline.
Sa et al. identified a distinct neuronal subpopulation that controls brown adipose tissue thermogenesis. In mice fed a high-fat diet, hypothalamic GABRA5 neurons are deactivated by GABA released by surrounding astrocytes and inhibition of GABA synthesis ameliorates diet-induced obesity.
The stress associated with early-life social deprivation in mice results in corticosterone-driven overstimulation of cortical synapse removal by astrocytes and behavioural abnormalities in mature animals.
Human glial progenitors transplanted into a chimeric mouse brain replace sick or older human glia, a finding that could one day lead to new treatments for neurological disease.