Researchers discover the SELK neuron, a single-cell decision-maker in fruit flies that weighs sweet vs. bitter signals to determine whether to eat or flee.
Category: neuroscience – Page 9
Blood-brain barrier disruption, traumatic encephalopathy, and cognitive decline in retired athletes
Traumatic head injuries from collision and combat sports disrupt the blood-brain barrier and trigger inflammation for years after retirement, shows a new MRI and transcriptomic analysis of retired athletes.
Find out more in Science TranslationalMedicine.
Sci. Transl. Med. 18, eadu6037 (2026). DOI:10.1126/scitranslmed.adu6037
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Synaptic connectivity alone can reveal neuron types
Recent technological advances facilitate the reconstruction of complete brain connectomes in small organisms and partial connectomes in mammals, involving the mapping of the network of neurons and synaptic connections. Accurate cell typing of these connectomes aids in interpreting circuit functions and comparing brain organization across species.
Traditionally, cell typing relied on manual morphological classification by experts—a slow process that required detailed anatomical information. However, morphology can be deceptive or inadequate in many brain regions, especially in circuits with repeated cell types, where neurons can share very similar morphology despite differing in connectivity.
Frontiers: Information storage and transfer in the brain require a high computational power
Neuronal network display various local or global mechanisms to allow information storage and transfer in the brain. From synaptic to intrinsic plasticity, the rules of input–output function modulation have been well characterized in neurons. In the past years, astrocytes have been suggested to increase the computational power of the brain and we are only just starting to uncover their role in information processing. Astrocytes maintain a close bidirectional communication with neurons to modify neuronal network excitability, transmission, axonal conduction, and plasticity through various mechanisms including the release of gliotransmitters or local ion homeostasis. Astrocytes have been significantly studied in the context of long-term or short-term synaptic plasticity, but this is not the only mechanism involved in memory formation. Plasticity of intrinsic neuronal excitability also participates in memory storage through regulation of voltage-gated ion channels or axonal morphological changes. Yet, the contribution of astrocytes to these other forms of non-synaptic plasticity remains to be investigated. In this review, we summarized the recent advances on the role of astrocytes in different forms of plasticity and discuss new directions and ideas to be explored regarding astrocytes-neuronal communication and regulation of plasticity.
The rules governing changes in synaptic and intrinsic plasticity are diverse and complex, sometimes synergistic and sometimes not (Debanne et al., 2019). Most studies have been neuro-centric, despite growing evidence that astrocytes can intervene or interact to modify or modulate synaptic transmission (Araque et al., 1998; Jourdain et al., 2007; Bonansco et al., 2011), input integration, neuronal excitability (Tan et al., 2017), spike waveform or axonal conductivity (Sasaki et al., 2011; Lezmy et al., 2021). Astrocytes can detect neuronal activity, and depending on the firing rate of action potentials (APs), they can not only release gliotransmitters such as adenosine or glutamate (Hamilton et al., 2008; Lezmy et al., 2021), but also trigger intracellular calcium ([Ca2+]i) oscillations at different frequencies (Pasti et al., 1997).
Protein modification in neurodegenerative diseases
The graphical abstract showcases the diversity of posttranslational modifications (PTMs) influencing protein structure and function. It features schematic representations of the following 10 prominent PTMs: phosphorylation (addition of phosphate groups), acetylation (addition of acetyl groups), methylation (addition of methyl groups), SUMOylation (attachment of SUMO proteins), ubiquitylation (attachment of ubiquitin molecules), succinylation (addition of succinyl groups), S-nitrosylation (attachment of NO), ADP-ribosylation (addition of ADP-ribose groups), glycosylation (addition of sugar molecules), and palmitoylation (attachment of palmitate groups).
Locus coeruleus–amygdala circuit disrupts prefrontal control to impair fear extinction
One of the most-viewed PNAS articles in the last week is “Locus coeruleus–amygdala circuit disrupts prefrontal control to impair fear extinction.” Explore the article here: https://ow.ly/yFH250Ywubb.
For more trending articles, visit https://ow.ly/tZsG50Ywubg.
Stress undermines extinction learning and hinders exposure-based clinical therapies for a variety of neuropsychiatric disorders. In both animals and humans, dysfunction in the ventromedial prefrontal cortex (vmPFC) contributes to stress-impaired extinction, but the neural circuit by which stress modulates vmPFC function is not known. We hypothesize that locus coeruleus (LC) norepinephrine undermines extinction learning by recruiting projections from the basolateral amygdala (BLA) to vmPFC. Using a combination of circuit-specific chemogenetics and calcium imaging, we find that activation of LC noradrenergic neurons mimics a behavioral stressor (footshock), induces freezing behavior, reduces spontaneous neuronal activity in the vmPFC, impairs extinction learning, and alters the population dynamics of vmPFC ensembles.
Using mRNA to Fight Tau Aggregation in Alzheimer’s
Researchers publishing in Cell Reports Medicine have described the development of a lipid nanoparticle (LNP) that delivers mRNA to neurons in order to stop the formation of tau aggregates and fight Alzheimer’s disease.
Tau and amyloids
Amyloid beta deposition between neurons and tau aggregation within neurons are both hallmarks of Alzheimer’s disease, and evidence suggests that the latter is potentially more significant than the former [1]. While some potential therapies have been discovered that may disaggregate these tau tangles after they have formed [2], no therapy has yet been approved by the FDA to do this.
The Janus face of NK cells in neurodevelopment
NK cells in neurodevelopment.
Maternal immune activation (MIA) during pregnancy perturbs fetal neurodevelopment, with natural killer (NK) cells emerging as key contributors to neurodevelopmental disorders (NDDs) such as autism spectrum disorder (ASD).
Clinical studies consistently report NK cell dysfunction in ASD patients and their mothers, characterized by altered cytotoxicity, hyperactivation at rest, functional exhaustion on stimulation, and skewed receptor/genetic profiles.
Uterine NK (uNK) cells, indispensable for placental and fetal development, can paradoxically promote NDDs when hyperactivated, releasing granzyme B (GZMB) that disrupts fetal brain structure and function.
Elucidating the MIA-driven ‘uNK/ GZMB–microglia–NDD’ axis is essential to devise preventive strategies for high-risk pregnancies and identify early biomarkers of neurodevelopmental risk. sciencenewshighlights ScienceMission https://www.cell.com/cms/10.1016/j.it.2025.10.001/asset/89cd…ts/gr3.jpg https://sciencemission.com/Janus-face-of-NK-cells
Maternal immune activation (MIA), triggered by infection or inflammation during pregnancy, is a well-recognized risk factor for neurodevelopmental disorders (NDDs) such as autism spectrum disorder (ASD). Clinical cohort studies and rodent models suggest that natural killer (NK) cells play a significant role in NDD pathogenesis, but the underlying mechanisms remain poorly defined. Here, we summarize the key immune mediators involved in MIA-induced NDDs, emphasizing microglia as a central hub. We then examine emerging evidence implicating aberrant NK cell activation in ASD, underscoring their overlooked contribution to impaired neurodevelopment. Finally, we discuss potential mechanisms of NK cell–microglia crosstalk in NDDs. Elucidating these interactions in the context of MIA will be crucial for developing preventive and therapeutic strategies against inflammation-driven NDDs.