Adipose-brain axis in metabolic inflammation.

White adipose tissue (WAT) in addition to storing excess energy also releases cytokines, lipid mediators, adipokines, and extracellular vesicles that influence brain physiology.

The inflammatory mediators disrupt key brain interfaces, including the blood-brain barrier (BBB), perivascular and glymphatic clearance pathways, promoting endothelial dysfunction, altered astrocyte-pericyte support, impaired amyloid-b clearance, and region-specific glial activation.

In the brain, obesity-associated neuroinflammation leads to various neuronal dysfunction including cognition.

The authors discuss the role of adipokines in adipose-brain communication during obesity including how they contribute to neuroinflammation and synaptic dysfunction.

The authors also discuss therapeutic strategies targeting the adipose-brain axis, including exercise and dietary interventions and pharmacological approaches such as orlistat and incretin-based therapies. sciencenewshighlights ScienceMission https://sciencemission.com/adipose-brain-axis

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The Epstein-Barr virus (EBV) is one of the world’s most common viruses, thought to be lurking in 95 percent of adults. For most, it causes no obvious symptoms.

But EBV is more than a short-term infection.

Once it enters the body, EBV can stay for life, and it has been linked to several cancers, multiple sclerosis, and other severe health complications. Now, new research has given us a promising way to fight it.

Opening of the mitochondrial permeability transition pore, Ca2+ overload, and mitochondrial fragmentation are early features of stroke-induced brain injury observed in experimental models.

Mitochondrial reactive oxygen species and activation of the cyclophilin D– reactive oxygen species–NLR family pyrin domain-containing 3–matrix metalloproteinase-9 axis are associated with intracranial aneurysm progression, linking mitochondrial stress to vascular wall instability.

Disruption of mitochondrial homeostasis exacerbates vascular pathology in intracranial atherosclerotic stenosis, arteriovenous malformations, and cavernous malformation, indicating a shared mitochondrial contribution across cerebrovascular disorders.

Pharmacological modulation of mitochondrial permeability, redox signaling, proprotein convertase subtilisin/ kexin type 9, and mechanistic target of rapamycin kinase pathways shows robust preclinical efficacy, while clinical outcomes remain heterogeneous.

Experimental studies support the feasibility of mitochondrial transplantation in models of cerebrovascular injury, including stroke. sciencenewshighlights ScienceMission https://sciencemission.com/Mito-dysfunction-in-CVD

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Mitochondria are central regulators of cerebrovascular health through their control of energy metabolism, Ca2+ homeostasis, and redox signaling, and their dysfunction represents a convergent pathogenic mechanism across cerebrovascular diseases. In ischemic stroke, mitochondrial failure exacerbates neuronal injury via permeability transition pore opening, oxidative stress, and bioenergetic collapse, while altered mitochondrial dynamics and the release of mitochondrial damage-associated molecular patterns amplify neuroinflammation during reperfusion. Beyond stroke, mitochondrial dysfunction contributes to intracranial aneurysms, atherosclerotic stenosis, and vascular malformations, where oxidative stress, mitochondrial DNA instability, and cell type-specific metabolic reprogramming drive vascular remodeling and lesion progression.