Sex-based differences in the long-term fate of hippocampal neurons born after a traumatic brain injury

Frontiers in Behavioral Neuroscience, Journal Year: 2025, Volume and Issue: 19

Published: Feb. 5, 2025

Introduction Moderate-to-severe traumatic brain injury (TBI) results in an early loss of immature hippocampal granule cells and the activation typically quiescent neural stem (NSCs) dentate gyrus. Activation NSCs leads to a robust increase proliferation generation progenitor (NPCs), supporting restoration neuron population over period 1–2 weeks. However, it is unclear if neurons born after develop normally, survive long-term functionally integrate into network. Although adult neurogenesis regulated sex-dependent manner, majority pre-clinical TBI studies lack inclusion both sexes. The goal this study was examine sex differences response moderate controlled cortical impact injury. Methods In-vivo labeling NPCs tracking their morphological development cell achieved using inducible Cre recombinase driven by Ascl1 promoter CAG-floxStopTom reporter mouse. basic helix-loop-helix transcription factor transiently expressed activated gyrus mammalian brain. To specifically label acutely TBI, tamoxifen delivered mice on days 2 3 postinjury. Mice survived 6 weeks allow for full neuronal maturation tdTomato-labeled NPCs. Results At postinjury, numbers tdTomato-positive were significantly reduced ipsilateral hippocampus brain-injured compared controls, with more pronounced decrease males. Further, posttrauma-born males, but not females, exhibited impaired dendritic development. Neurons extended axons which formed synaptic terminals within CA3 region. Numbers mossy fiber boutons decreased injured males naïve or females. Potential forms plasticity observed including increased contralateral bouton volume. Together these data suggest neurogenic advantage females Discussion This first report posttraumatic demonstrate modification TBI.

Language: Английский

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Microbiota fasting-related changes ameliorate cognitive decline in obesity and boost ex vivo microglial function through the gut-brain axis

Gut, Journal Year: 2025, Volume and Issue: unknown, P. gutjnl - 335353

Published: May 7, 2025

Abstract Background Obesity-related cognitive decline is linked to gut microbiota dysbiosis, with emerging evidence suggesting that dietary interventions may ameliorate impairment via gut-brain axis modulation. The role of microglial cells in this process remains underexplored. Objective To investigate how diet-induced changes influence function individuals obesity and their activity, determine the impact specific interventions. Design This study included 96 participants who were randomised into three intervention groups: Mediterranean diet (Med), alternate-day fasting (ADF) ketogenic (Keto). Cognitive performance composition assessed pre-intervention post-intervention. effects microbiota-related on further evaluated mice models through faecal transplantation vitro model exosome treatment. Results Both Keto ADF groups demonstrated significant weight loss, but improved most notably group, association reduced inflammation. Diet-related was correlated outcomes human study. Mice confirmed benefits microbiota-dependent enhanced phagocytic capacity inflammation, accompanied by microglia morphology. Conclusion Fasting-induced modifications contribute improvement obesity, playing a crucial mediatory role. Among interventions, effectively performance, its potential as therapeutic strategy for obesity-related decline. Further studies are required fully elucidate underlying mechanisms. Trial registration number NCT04453150 .

Language: Английский

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The Role of Neuroinflammation in Shaping Neuroplasticity and Recovery Outcomes Following Traumatic Brain Injury: A Systematic Review

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(21), P. 11708 - 11708

Published: Oct. 31, 2024

Neuroplasticity and neuroinflammation are variables seen during recovery from traumatic brain injury (TBI), while biomarkers useful in monitoring guiding rehabilitation efforts. This systematic review examines how affects neuroplasticity following TBI animal models humans. Studies were identified an online search of the PubMed, Web Science, Embase databases without any time range. has been registered on Open OSF (n) UDWQM. Recent studies highlight critical role like serum amyloid A1 (SAA1) Toll-like receptor 4 (TLR4) predicting patients' severity outcomes, offering potential for personalized treatment improved neurorehabilitation strategies. Additionally, insights reveal recovery, emphasizing targets such as NOD-like family pyrin domain-containing 3 (NLRP3) microglia enhancing therapeutic interventions. emphasizes central TBI, its adverse impact suggests that targeted anti-inflammatory treatments biomarker-based approaches hold key to improvement. Such will need further development future research by integrating neuromodulation pharmacological interventions, along with biomarker validation, optimize management TBI.

Language: Английский

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Biomarkers of Brain Cell-Specific Immune Mechanisms and Their Translational Potential: State of the Evidence for Traumatic Brain Injury

Neurochemical Journal, Journal Year: 2024, Volume and Issue: 18(4), P. 752 - 762

Published: Dec. 1, 2024

Language: Английский

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