A5026294090- Neuroscience and Neuropharmacology Research
- Diet and metabolism studies
- Ion channel regulation and function
- Epilepsy research and treatment
- Neuroinflammation and Neurodegeneration Mechanisms
- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- Calpain Protease Function and Regulation
- Ginkgo biloba and Cashew Applications
- Amino Acid Enzymes and Metabolism
- Diet, Metabolism, and Disease
- Neurological Disease Mechanisms and Treatments
- Neurological and metabolic disorders
- Genetic Neurodegenerative Diseases
- Metabolism and Genetic Disorders
- Diabetes Management and Research
- Neurological disorders and treatments
- Pancreatic function and diabetes
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- COVID-19 Clinical Research Studies
- Molecular Sensors and Ion Detection
- Tryptophan and brain disorders
- GABA and Rice Research
- Alzheimer's disease research and treatments
- Heart Rate Variability and Autonomic Control
Universidad Nacional Autónoma de México
2011-2023
Universidad Rey Juan Carlos
2020
Hospital Universitario Rey Juan Carlos
2020
Instituto Nacional de Cardiología
1991-2016
Instituto Nacional de Neurología y Neurocirugía
1990
Mitochondrial activity and quality control are essential for neuronal homeostasis as neurons rely on glucose oxidative metabolism. The ketone body, D-β-hydroxybutyrate (D-BHB), is metabolized to acetyl-CoA in brain mitochondria used an energy fuel alternative glucose. We have previously reported that D-BHB sustains ATP production stimulates the autophagic flux under deprivation neurons; however, effects of mitochondrial turnover physiological conditions still unknown. Sirtuins (SIRTs)...
Glucose is the main energy substrate in brain but certain circumstances such as prolonged fasting and suckling period alternative substrates can be used ketone bodies (KB), beta-hydroxybutyrate (BHB), acetoacetate. It has been shown that KB prevent neuronal death induced during limiting conditions excitotoxicity. The protective effect of mainly attributed to improvement mitochondrial function. In present study, we have investigated D-BHB against by severe noncoma hypoglycemia rat vivo...
Prolonged activation of glutamate receptors leads to excitotoxicity. Several processes such as reactive oxygen species (ROS) production and the calcium-dependent protease, calpain, contribute glutamate-induced damage. It has been suggested that ROS-producing enzyme, NADPH oxidase (NOX), plays a role in Studies have reported NOX after NMDA receptor stimulation during excitotoxic damage, but non-NMDA metabotropic is unknown. We evaluated roles different subtypes on neuronal death induced by...
Abstract Autophagy is triggered during nutrient and energy deprivation in a variety of cells as homeostatic response to metabolic stress. In the CNS, deficient autophagy has been implicated neurodegenerative diseases ischemic brain injury. However, its role hypoglycemic damage poorly understood dynamics glucose reperfusion periods, not fully described. present study, we analyzed changes content proteins BECN1, LC3-II p62/SQSTM1 by western blot, autophagosome formation was followed through...
Abstract Ischemic stroke is a leading cause of disability worldwide. There no simple treatment to alleviate ischemic brain injury, as thrombolytic therapy applicable within narrow time window. During the last years, ketogenic diet (KD) and exogenous administration ketone body β‐hydroxybutyrate (BHB) have been proposed therapeutic tools for acute neurological disorders both can reduce injury. However, mechanisms involved are not completely clear. We previously shown that D enantiomer BHB...
During excitotoxic damage, neuronal death results from the increase in intracellular calcium, induction of oxidative stress, and a subsequent inflammatory response. NADPH oxidases (NOX) are relevant sources reactive oxygen species (ROS) during damage. oxidase-2 (NOX-2) has been particularly related to damage death, as well resolution As ROS crucial components regulation response, this work, we evaluated role NOX-2 progression inflammation resulting glutamate-induced striatum an vivo...
Background: The ketone bodies (KB), β-hydroxybutyrate (BHB) and acetoacetate, have been proposed for the treatment of acute chronic neurological disorders, however, molecular mechanisms involved in KB protection are not well understood. can substitute glucose support mitochondrial metabolism increasing cell survival. We reported that D-isomer BHB (D-BHB) stimulates autophagic degradation during deprivation cultured neurons viability. Autophagy is a lysosomal process damaged proteins...
Moderate recurrent hypoglycemia (RH) is frequent in Type 1 diabetes mellitus (TIDM) patients who are under intensive insulin therapy increasing the risk for severe (SH). The consequences of RH not well understood and its repercussions on neuronal damage cognitive function after a subsequent episode SH have been poorly investigated. In current study, we addressed this question observed that previous during seven consecutive days exacerbated oxidative death induced by accompanied short period...
Glucose supply from blood is mandatory for brain functioning and its interruption during acute hypoglycemia or cerebral ischemia leads to injury. Alternative substrates glucose such as the ketone bodies (KB), acetoacetate (AcAc), β-hydroxybutyrate (BHB), can be used energy fuels in prevent neuronal death, but mechanisms involved are still not well understood. During deprivation adaptive cell responses activated autophagy, a lysosomal-dependent degradation process, support survival. However,...