BUSCADOR RECOLECTA

<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>

<p>Stroke is a major public health concern, whit limited clinically approved interventions available to enhance sensorimotor recovery beyond reperfusion. Remarkably, spontaneous recovery is observed in certain stroke patients, suggesting the existence of a self-brain repair mechanism not yet fully understood. In a rat model of permanent cerebral ischemia, we described an increase in oligodendrocytes expressing 3RTau in damaged area. Considering that restoration of myelin integrity ameliorates symptoms in many neurodegenerative diseases, here we hypothesize that this cellular response could trigger remyelination. Our results revealed after ischemia an early recruitment of OPCs to damaged area, followed by their differentiation into 3RTau+ pre-myelinating cells and subsequent into remyelinating oligodendrocytes. Using rat brain slices and mouse primary culture we confirmed the presence of 3RTau in pre-myelinating oligodendrocytes and a subset of mature. The myelin status analysis confirmed long-term remyelination in the damaged area. Postmortem samples from stroke subjects showed a reduction in oligodendrocytes, 3RTau+ cells, and myelin complexity in subcortical white matter. In conclusion, the dynamics of oligodendrocytes populations after ischemia reveals a spontaneous brain self-repair mechanism which restores the functionality of neuronal circuits long-term by remyelination of damage area. This is evidenced by the improvement of sensorimotor functions in ischemic rats. A deep understanding of this mechanism could be valuable in the search for alternative oligodendrocyte-based, therapeutic interventions to reduce the effects of stroke.</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.
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In this review, we provide recent data on the role of mTOR kinase in the brain under physiological conditions and after damage, with a particular focus on cerebral ischemia. We cover the upstream and downstream pathways that regulate the activation state of mTOR complexes. Furthermore, we summarize recent advances in our understanding of mTORC1 and mTORC2 status in ischemia–hypoxia at tissue and cellular levels and analyze the existing evidence related to two types of neural cells, namely glia and neurons. Finally, we discuss the potential use of mTORC1 and mTORC2 as therapeutic targets after stroke., This article was funded by grant from Spanish Ministry of Science and Innovation through grant PID2020-115876GB-I00. G.M.-L. is supported by a grant from Fundación Tatiana Pérez de Guzmán el Bueno. The funders had no role in decision to publish, or preparation of the manuscript

descripción no proporcionada por scopus, This work was funded by grants from Departamento de Biología, Facultad de Ciencias-Universidad Autónoma de Madrid (BIOUAM03-2020) and Spanish Ministry of Science and Innovation (PID2020-115876GB-I00) (to MJPA). The funders had no role in decision to publish, or preparation of the manuscript.

Stroke is a major public health concern, with limited clinically approved interventions available to enhance sensorimotor recovery beyond reperfusion. Remarkably, spontaneous recovery is observed in certain stroke patients, suggesting the existence of a brain self-repair mechanism not yet fully understood. In a rat model of permanent cerebral ischemia, we described an increase in oligodendrocytes expressing 3RTau in damaged area. Considering that restoration of myelin integrity ameliorates symptoms in many neurodegenerative diseases, here we hypothesize that this cellular response could trigger remyelination. Our results revealed after ischemia an early recruitment of OPCs to damaged area, followed by their differentiation into 3RTau pre-myelinating cells and subsequent into remyelinating oligodendrocytes. Using rat brain slices and mouse primary culture we confirmed the presence of 3RTau in pre-myelinating and a subset of mature oligodendrocytes. The myelin status analysis confirmed long-term remyelination in the damaged area. Postmortem samples from stroke subjects showed a reduction in oligodendrocytes, 3RTau cells, and myelin complexity in subcortical white matter. In conclusion, the dynamics of oligodendrocyte populations after ischemia reveals a spontaneous brain self-repair mechanism which restores the functionality of neuronal circuits long-term by remyelination of damaged area. This is evidenced by the improvement of sensorimotor functions in ischemic rats. A deep understanding of this mechanism could be valuable in the search for alternative oligodendrocyte-based, therapeutic interventions to reduce the effects of stroke., his article was funded by a grant from the Spanish Ministry of Science and Innovation (PID2020-115876GB-I00). G.M. is supported by a grant from Fundación Tatiana Pérez de Guzmán el Bueno, Peer reviewed

The mTORC1 and AMPK signalling pathways are considered key nodes regulating anabolism and catabolism, and they are altered in certain processes of neurodegeneration such as hypoxia associated with ischemic stroke or Alzheimer's disease. The lack of oxygen and/or glucose (oxygen and glucose deprivation-OGD) may affect the equilibrium of the mTORC1/AMPK pathways, perhaps aggravating neurodegeneration. The alteration of these pathways mediated by OGD may be reflected in other alterations, such as the activation of autophagy that could in turn modify the secretion/accumulation of amyloid-β, one of the two histopathological markers of Alzheimer's disease. Accordingly, we set out to analyze whether OGD enhances autophagy and its implication in neuronal amyloidosis. The data obtained reveal that OGD significantly dampens not only neuronal amyloid-β production but also, the total APP protein levels, without affecting BACE-1 levels. We show that this mechanism is independent of cellular proteolysis (autophagy or proteasome) and that it can be partially recovered by inhibiting HIF-1α activity., This work was supported by grants from the Spanish FEDER/Science and Innovation Ministry Proyectos I + D + i-RETOS-PID2021-124801NB-I00 and I + D + i-RETOS-PID2020-115876 GB-I00, This work was supported by grants from the Spanish FEDER/Science and Innovation Ministry Proyectos I + D + i-RETOS-PID2021-124801NB-I00, (FW) and I + D + i-RETOS-PID2020-115876 GB-I00 (MJP). This work was partially supported by Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED; an initiative of the ISCIII) [PI2016/01] (FW); and institutional grants from the Fundación Ramón Areces and Banco Santander to the CBMSO. In addition, MGJ was supported by a Predoctoral fellowship (Ref #FPU18/05727) and LO was initially supported by a Postdoctoral Contract from CIBERNED., Peer reviewed