A5012360866- Traumatic Brain Injury and Neurovascular Disturbances
- Mitochondrial Function and Pathology
- Traumatic Brain Injury Research
- Stress Responses and Cortisol
- Neuroendocrine regulation and behavior
- Cardiac Arrest and Resuscitation
- Vagus Nerve Stimulation Research
- Endoplasmic Reticulum Stress and Disease
- Nicotinic Acetylcholine Receptors Study
- Anesthesia and Neurotoxicity Research
- Neuroscience and Neuropharmacology Research
- Sepsis Diagnosis and Treatment
- Autophagy in Disease and Therapy
- Botulinum Toxin and Related Neurological Disorders
- Metabolism, Diabetes, and Cancer
- Stroke Rehabilitation and Recovery
- Genetics and Neurodevelopmental Disorders
- Neurogenesis and neuroplasticity mechanisms
- S100 Proteins and Annexins
- Pancreatic function and diabetes
- Neurological and metabolic disorders
- Child Development and Digital Technology
- Advanced Neuroimaging Techniques and Applications
- Trauma, Hemostasis, Coagulopathy, Resuscitation
- ATP Synthase and ATPases Research
The University of Texas Health Science Center at Houston
2013-2024
Southern Illinois University Carbondale
2015-2022
The University of Texas at Austin
2015
Institute of Neurobiology
2013
The perineuronal net (PNN) surrounds neurons in the central nervous system and is thought to regulate developmental plasticity. A few studies have shown an involvement of PNN hippocampal plasticity memory storage adult animals. In addition hippocampus, medial prefrontal cortex (mPFC) has been demonstrated be critical for long-term memory, particularly memories temporally separated events. present study, we examined role acquisition retention trace (in which conditioned unconditioned stimuli...
Mitochondrial function is intimately linked to cellular survival, growth, and death. Mitochondria not only generate ATP from oxidative phosphorylation, but also mediate intracellular calcium buffering, generation of reactive oxygen species (ROS), apoptosis. Electron leakage the electron transport chain, especially damaged or depolarized mitochondria, can excess free radicals that damage proteins, DNA, lipids. Furthermore, mitochondrial releases pro-apoptotic factors initiate cell Previous...
The majority of people who sustain a traumatic brain injury (TBI) have an that can be classified as mild (often referred to concussion). Although head CT scans for most subjects sustained TBI (mTBI) are negative, these persons may still suffer from neurocognitive and neurobehavioral deficits. In order expedite pre-clinical research develop therapies, there is need well-characterized animal models mTBI reflect the neurological, neurocognitive, pathological changes seen in human patients....
Traumatic brain injury (TBI) is a major human health concern that has the greatest impact on young men and women. The breakdown of blood–brain barrier (BBB) an important pathological consequence TBI initiates secondary processes, including infiltration inflammatory cells, which can exacerbate inflammation contribute to poor outcome. While role within injured been examined in some detail, contribution peripheral/systemic pathophysiology largely unknown. Recent studies have implicated vagus...
Adult hippocampal neurogenesis has been shown to be required for certain types of cognitive function. For example, studies have that these neurons are critical pattern separation, the ability store similar experiences as distinct memories. Although traumatic brain injury (TBI) cause loss newborn neurons, signaling pathway(s) triggers their death is unknown. Endoplasmic reticulum (ER) stress activates PERK-eIF2α pathway acts restore ER function and improve cell survival. However,...
Acetylcholine is an excitatory neurotransmitter in the central nervous system that plays a key role cognitive function, including learning and memory. Previous studies have shown experimental traumatic brain injury (TBI) reduces cholinergic neurotransmission, decreases evoked release of acetylcholine, alters receptor levels. Galantamine (U.S. Food Drug Administration approved for treatment vascular dementia Alzheimer's disease) has been to inhibit acetylcholinesterase activity allosterically...
Intravenous administration of bone marrow derived mesenchymal stem cells (MSCs) has been shown to reduce blood brain barrier compromise and improve neurocognition following traumatic injury (TBI). These effects occur in the absence engraftment differentiation these injured brain. Recent studies have that soluble factors produced by MSCs mediate a number therapeutic effects. In this study, we sought determine if intravenous (IV-MSCs) could enhance hippocampal neurogenesis TBI. Our results...
Abstract Prolonged metabolic suppression in the brain is a well‐characterized secondary pathology of both experimental and clinical traumatic injury ( TBI ). AMP ‐activated kinase AMPK ) acts as cellular energy sensor that, when activated, regulates various catabolic pathways to decrease ATP consumption increase synthesis. As availability after suppressed, we questioned if increasing activity would improve cognitive outcome. was delivered using electromagnetic controlled cortical impact...
Mesenchymal stem cells (MSCs) have been shown to potent therapeutic effects in a number of disorders including traumatic brain injury (TBI). However, the molecular mechanism(s) underlying these protective are largely unknown. Herein we demonstrate that tissue inhibitor matrix metalloproteinase-3 (TIMP3), soluble protein released by MSCs, is neuroprotective and enhances neuronal survival neurite outgrowth vitro. In vivo murine model TBI, intravenous recombinant TIMP3 dendritic abrogates loss...
Patients who survive traumatic brain injury (TBI) are often faced with persistent memory deficits. The hippocampus, a structure critical for learning and memory, is vulnerable to TBI its dysfunction has been linked impairments. Protein kinase RNA-like ER regulates protein synthesis (by phosphorylation of eukaryotic initiation factor 2 alpha [eIF2α]) in response endoplasmic reticulum (ER) stressors, such as increases calcium levels, oxidative damage, energy/glucose depletion, all which have...
Abstract A hallmark of long‐term memory formation is the requirement for protein synthesis. Administration synthesis inhibitors impairs without influencing short‐term memory. Rapamycin a specific inhibitor target rapamycin complex 1 (TORC1) that has been shown to block and impair In addition regulating synthesis, TORC1 also phosphorylates Unc‐51‐like autophagy activating kinase‐1 (Ulk‐1) suppress autophagy. As can be activated by (and inhibits memory), our aim was test hypothesis would...
Concussive force can cause neurocognitive and neurobehavioral dysfunction by inducing functional, electrophysiological, and/or ultrastructural changes within the brain. Although concussion-triggered symptoms typically subside days to weeks in most people, 15%–20% of cases, symptomology continue beyond this time point. Problems with memory, attention, processing speed, cognitive flexibility (e.g., problem solving, conflict resolution) are some prominent post-concussive symptoms. Repeated...
Epidemiology studies have found that a comorbidity exists between traumatic brain injury (TBI) and stress-related disorders. However, the anatomical cellular bases for this association is poorly understood. An inability to extinguish memory of event lies at core many Experimental shown medial pre-frontal cortex (mPFC), especially infralimbic (IL) cortex, required extinction storing extinction. The output from central nucleus amygdala projects lateral hypothalamus, paraventricular nucleus,...
Some of the prominent features long-term memory formation include protein synthesis, gene expression, enhanced neurotransmitter release, increased excitability, and new synapses. As these processes are critically dependent on mitochondrial function, we hypothesized that respiration dynamics would play a role in formation. To address this possibility, measured oxygen consumption (OCR) hippocampal tissue punches from trained untrained animals. Our results show context fear training...
The leading cause of death in the juvenile population is trauma, and particular neurotrauma. brain response to neurotrauma not completely understood. Endoplasmic reticulum (ER) stress has been shown contribute injury expansion behavioral deficits adult rodents furthermore seen postmortem human brains diagnosed with chronic traumatic encephalopathy. Whether endoplasmic increased juveniles (TBI) poorly delineated. We investigated this important topic using a rat controlled cortical impact...
The prevalence of mild traumatic brain injury (mTBI) is high compared with moderate and severe TBI, comprising almost 80% all injuries. mTBI activates a complex cascade biochemical, molecular, structural, pathological changes that can result in neurological cognitive impairments. These impairments manifest even the absence overt damage. Given complexity triggered by mTBI, combination drugs target multiple TBI-activated cascades may be required to improve outcomes. It has been previously...
Extensive research with rodent models has shown detrimental effects of early-life adversity (ELA) on behavioral (e.g., impulsive behavior, anxiety, and depression) neurobiological processes alterations neuroendocrine maturation brain areas). However, heterogeneous methodologies, including types variations ELA manipulations could have contributed to inconsistent findings across studies. Maternal separation (MS) limited bedding/nesting (LBN) are widely implemented protocols. Orso et al. [1]...