Core Viewpoint - The article discusses the significant impact of high fructose consumption, particularly during early life, on neurodevelopment and the potential increase in anxiety disorders in adolescents. It highlights the mechanisms by which fructose affects microglial function and brain development, emphasizing the role of the GLUT5 protein in this process [1][3][11]. Group 1: Fructose Consumption and Health Implications - Fructose is a common sugar that has been widely used in food and beverages, often perceived as a "healthy sugar" due to its low glycemic index and high sweetness [1]. - Over the past 50 years, fructose consumption has surged, primarily due to the use of high fructose corn syrup in processed foods and drinks, which is linked to metabolic diseases such as obesity, diabetes, and fatty liver [1][6]. - Excessive fructose intake has also been associated with an increased risk of colorectal cancer and anxiety disorders, particularly among adolescents [1][6]. Group 2: Research Findings on Fructose and Neurodevelopment - A study published in Nature indicates that high fructose intake during early life impairs microglial phagocytosis and neurodevelopment, potentially leading to increased anxiety risk later in life [2][3][11]. - The research found that high fructose consumption significantly reduces the phagocytic activity of microglial cells in the brains of young mice, which is crucial for clearing dead neurons and ensuring proper brain development [5][7]. - The negative effects of high fructose on brain function are mediated by the GLUT5 protein, which is responsible for fructose transport into cells. The absence of GLUT5 can reverse the adverse effects of high fructose on microglial function [7][9]. Group 3: Implications for Dietary Habits - The findings suggest that early life exposure to high fructose may lead to cognitive deficits and anxiety-like behaviors during adolescence, highlighting the importance of dietary choices during pregnancy and early childhood [9][16]. - The research team is exploring fructose analogs as potential substitutes to mitigate the negative impacts of fructose in modern diets, acknowledging the challenges in changing dietary habits [12][13].

Core Viewpoint - The article highlights the significant contributions of Professor Danyang in the field of sleep research and her recent affiliation with Shenzhen Medical Academy, where she will establish a Sleep and Consciousness Laboratory [1][4]. Group 1: Professor Danyang's Background - Professor Danyang graduated from Peking University with a degree in Physics and later pursued a PhD in Biology at Columbia University, followed by postdoctoral research at Rockefeller University and Harvard Medical School [4]. - She has been a faculty member at the University of California, Berkeley since 1997, focusing on the neural circuits that control sleep and the functions of the prefrontal cortex [4][21]. Group 2: Recent Research Contributions - On December 8, 2023, Professor Danyang's team published a study in Cell, revealing that frontal cortical ignition, related to consciousness awareness, is strongly suppressed during NREM sleep in mice due to cholinergic modulation [7][10]. - On January 18, 2024, a study published in Nature Neuroscience demonstrated that microglia can promote sleep through calcium-dependent modulation of norepinephrine transmission, suggesting a protective role for microglia in brain health [12][13]. - On January 17, 2025, a study in Science Advances explored how activation of locus coeruleus noradrenergic neurons rapidly increases homeostatic sleep pressure, indicating a mechanism for sleep regulation [15][17]. Group 3: Implications for Sleep Research - The findings from Professor Danyang's research suggest that understanding the mechanisms of sleep regulation could have implications for addressing sleep disruptions associated with neurodegenerative diseases like Alzheimer's [13]. - The research emphasizes the importance of microglial function in maintaining sleep and brain homeostasis, potentially offering insights into therapeutic strategies for sleep-related disorders [13]. - The studies collectively indicate that the functional fatigue of locus coeruleus neurons may lead to increased sleep pressure, providing a new perspective on the relationship between wakefulness and sleep [17].

Core Viewpoint - The study reveals that maternal immune activation due to viral infection leads to abnormal secretion of extracellular granzyme B (GzmB) by natural killer (NK) cells, which crosses the maternal-fetal barrier, resulting in the accumulation of fetal macrophages and activation of microglia, ultimately causing neurodevelopmental disorders and behavioral defects in offspring [2][3][6]. Group 1: Research Findings - Maternal NK cells activated by viral infection promote the accumulation of activated macrophages in the fetal brain, leading to neurodevelopmental disorders and behavioral defects in offspring [3][6]. - Extracellular granzyme B (GzmB) is released by maternal CD49a+ tissue-resident NK cell subsets under type I interferon stimulation, crossing the maternal-fetal barrier and promoting the accumulation of fetal macrophages expressing interferon-stimulated genes (ISG) and activation of microglia [3][6]. - Targeting extracellular GzmB by systemic administration of serine protease inhibitor Serpina3n or knocking out the GzmB gene in maternal NK cells can alleviate neuroimmune disorders in the fetal brain induced by maternal immune activation [3][6]. Group 2: Implications - The findings indicate that exposure to a disrupted maternal environment reprograms the immune function of decidual NK cells, disrupting the neuroimmune balance in the fetus and increasing the risk of neurodevelopmental disorders in offspring [6].

Core Viewpoint - The study reveals that exosomes derived from macrophage-derived foam cells in atherosclerotic plaques exacerbate ischemic white matter injury and vascular cognitive impairment by transmitting metabolic defects to microglia [2][5][10]. Group 1: Research Findings - Atherosclerosis (AS) is identified as an independent risk factor for vascular cognitive impairment (VCI), with unclear mechanisms [2]. - The research team discovered that exosomes in the circulation of AS patients worsen ischemic white matter injury and VCI [5]. - Foam cells produce exosomes that target microglia in the central nervous system, transmitting oxidative stress imbalance and metabolic defects through the miR-101-3p-Nrf2-Slc2a1 signaling axis [5][7]. Group 2: Potential Therapeutic Targets - The study confirms that inhibiting miR-101-3p or activating Nrf2 can counteract the effects of atherosclerotic exosomes and improve vascular cognitive impairment [6][7]. - The findings suggest a long-distance connection between peripheral macrophages and microglia, providing new insights and potential therapeutic targets for atherosclerosis-induced vascular cognitive impairment [3][10].