Publications by authors named "Benjamin A Devlin"
Article Synopsis
- * Glial cells are essential in forming cortical circuits and influencing how neurons adapt during critical stages of development.
- * The review emphasizes that the maturation of neuronal circuits involves communication between glial cells and neurons, suggesting a more complex interaction than previously understood.
Maternal immune activation is associated with adverse offspring neurodevelopmental outcomes, many mediated by in utero microglial programming. As microglia remain inaccessible throughout development, identification of noninvasive biomarkers reflecting fetal brain microglial programming could permit screening and intervention. We used lineage tracing to demonstrate the shared ontogeny between fetal brain macrophages (microglia) and fetal placental macrophages (Hofbauer cells) in a mouse model of maternal diet-induced obesity, and single-cell RNA-seq to demonstrate shared transcriptional programs.
View Article and Find Full Text PDFNeuron-microglia interactions dictate the development of neuronal circuits in the brain. However, the factors that support and broadly regulate these processes across developmental stages are largely unknown. Here, we find that IL34, a neuron-derived cytokine, is upregulated in development and plays a critical role in supporting and maintaining neuroprotective, mature microglia in the anterior cingulate cortex (ACC) of mice.
View Article and Find Full Text PDFMaternal immune activation is associated with adverse offspring neurodevelopmental outcomes, many mediated by in utero microglial programming. As microglia remain inaccessible throughout development, identification of noninvasive biomarkers reflecting fetal brain microglial programming could permit screening and intervention. We used lineage tracing to demonstrate the shared ontogeny between fetal brain macrophages (microglia) and fetal placental macrophages (Hofbauer cells) in a mouse model of maternal diet-induced obesity, and single-cell RNA-seq to demonstrate shared transcriptional programs.
View Article and Find Full Text PDFArticle Synopsis
- Air pollution and stress during pregnancy can cause problems in how baby boys behave, which may help explain some cases of autism.
- Mice studies show that when mothers are exposed to diesel exhaust and experience stress, their male babies have different brain cell shapes and changes in a part of the brain that affects feelings and behavior.
- The gut microbiome (the bacteria in our stomach) also changes in these male mice, and fixing those bacteria at birth can help stop some of the behavior issues caused by pollution and stress.
High maternal weight is associated with detrimental outcomes in offspring, including increased susceptibility to neurological disorders such as anxiety, depression and communicative disorders. Despite widespread acknowledgement of sex biases in the development of these disorders, few studies have investigated potential sex-biased mechanisms underlying disorder susceptibility. Here, we show that a maternal high-fat diet causes endotoxin accumulation in fetal tissue, and subsequent perinatal inflammation contributes to sex-specific behavioural outcomes in offspring.
View Article and Find Full Text PDFMany instances of sickness critically involve the immune system. The immune system talks to the brain in a bidirectional loop. This discourse affords the immune system immense control, such that it can influence behavior and optimize recovery from illness.
View Article and Find Full Text PDFArticle Synopsis
- - Understanding ALS mechanisms, particularly mitochondrial dysfunction, is key for developing new treatments, as prior studies indicate a critical link between mitochondrial issues and disease progression.
- - Hyperphosphorylated tau (pTau-S396) was found to mis-localize in ALS patients, leading to increased oxidative stress and mitochondrial fragmentation, which could impair cell function.
- - Reducing tau levels using a selective tau degrader showed potential in preventing mitochondrial dysfunction and oxidative stress in ALS models, suggesting a novel therapeutic pathway.