Pharmacological inhibition of mTORC1 reduces neural death and damage volumen after MCAO by modulating microglial reactivity

<p>Ischemic stroke is a sudden and acute disease characterized by neuronal death, increment of reactive gliosis (reactive microglia and astrocytes), and a severe inflammatory process. Neuroinflammation is an early event after cerebral ischemia, with microglia playing a leading role. Reactive microglia involve functional and morphological changes that drive a wide variety of phenotypes. In this context, deciphering the molecular mechanisms underlying such reactive microglial is essential to devise strategies to protect neurons and maintain certain brain functions affected by early neuroinflammation after ischemia. Here, we studied the role of mammalian target of rapamycin (mTOR) activity in the microglial response using a murine model of cerebral ischemia in the acute phase. We also determined the therapeutic relevance of the pharmacological administration of rapamycin, a mTOR inhibitor, before and after ischemic injury. Our data show that rapamycin, administered before or after brain ischemia induction, reduced the volume of brain damage and neuronal loss by attenuating the microglial response. Therefore, our findings indicate that the pharmacological inhibition of mTORC1 in the acute phase of ischemia may provide an alternative estrategia to reduce neuronal damage through attenuation of the associated neuroinflammation.</p>
<p>This dataset contains the raw data of cuantificación used in this study. It includes all the observations and measurements that were collected, which are essential for analysis and interpretation. The data is organized in a way that facilitates further exploration and analysis, ensuring that researchers can effectively utilize it for their own studies.</p>