Possible Implications of Obesity-Primed Microglia that Could Contribute to Stroke-Associated Damage

Microglia, the resident macrophages of the central nervous system, are essential players during physiological and pathological processes. Although they participate in synaptic pruning and maintenance of neuronal circuits, microglia are mainly studied by their activity modulating inflammatory environment and adapting their phenotype and mechanisms to insults detected in the brain parenchyma. Changes in microglial phenotypes are reflected in their morphology, membrane markers, and secreted substances, stimulating neighbor glia and leading their responses to control stimuli. Understanding how microglia react in various microenvironments, such as chronic inflammation, made it possible to establish therapeutic windows and identify synergic interactions with acute damage events like stroke. Obesity is a low-grade chronic inflammatory state that gradually affects the central nervous system, promoting neuroinflammation development. Obese patients have the worst prognosis when they suffer a cerebral infarction due to basal neuroinflammation, then obesity-induced neuroinflammation could promote the priming of microglial cells and favor its neurotoxic response, potentially worsening patients' prognosis. This review discusses the main microglia findings in the obesity context during the course and resolution of cerebral infarction, involving the temporality of the phenotype changes and balance of pro- and anti-inflammatory responses, which is lost in the swollen brain of an obese subject.

Automated summary

Microglia play important roles in physiological and pathological processes in the central nervous system. They are mainly studied for their ability to modulate inflammatory environment and adapt to insults in the brain. Understanding the reactions of microglia in various microenvironments, such as chronic inflammation, is crucial for developing therapeutic strategies. In the context of obesity, neuroinflammation caused by obesity can promote the activation of microglial cells and exacerbate their neurotoxic responses, potentially worsening patients' prognosis.