Pablo M. Casillas‐Espinosa

ORCID: 0000-0002-6199-9415
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About
Contact & Profiles
Research Areas
  • Epilepsy research and treatment
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Neuroscience and Neuropharmacology Research
  • Traumatic Brain Injury Research
  • Ion channel regulation and function
  • Neonatal and fetal brain pathology
  • S100 Proteins and Annexins
  • Pharmacological Effects and Toxicity Studies
  • Mitochondrial Function and Pathology
  • EEG and Brain-Computer Interfaces
  • Trace Elements in Health
  • Advanced Neuroimaging Techniques and Applications
  • Cardiac Arrest and Resuscitation
  • Diet and metabolism studies
  • Cerebrospinal fluid and hydrocephalus
  • Advanced MRI Techniques and Applications
  • Selenium in Biological Systems
  • Cardiac electrophysiology and arrhythmias
  • Neural dynamics and brain function
  • Drug Transport and Resistance Mechanisms
  • Computational Drug Discovery Methods
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Genetics and Neurodevelopmental Disorders
  • Alzheimer's disease research and treatments
  • Stress Responses and Cortisol

Monash University
2018-2025

The Royal Melbourne Hospital
2017-2025

The University of Melbourne
2015-2025

The Alfred Hospital
2018-2025

Alfred Health
2019-2025

Discovery Institute
2022-2023

Austin Hospital
2022

Monash Medical Centre
2022

Austin Health
2022

Royal Hallamshire Hospital
2022

Epilepsy after pediatric traumatic brain injury (TBI) is associated with poor quality of life. This study aimed to characterize post-traumatic epilepsy in a mouse model injury, and evaluate the role interleukin-1 (IL-1) signaling as target for pharmacological intervention. Male mice received controlled cortical impact or sham surgery at postnatal day 21, approximating toddler-aged child. Mice were treated acutely an IL-1 receptor antagonist (IL-1Ra; 100 mg/kg, s.c.) vehicle. Spontaneous...

10.1523/jneurosci.0982-17.2017 article EN Journal of Neuroscience 2017-07-19

There are no pharmacological disease-modifying treatments with an enduring effect to mitigate the seizures and comorbidities of established chronic temporal lobe epilepsy (TLE). This study aimed evaluate for disease modifying effects sodium selenate treatment in chronically epileptic rat post-status epilepticus (SE) model drug-resistant TLE. Wistar rats underwent kainic acid-induced SE or sham. Ten-weeks post-SE, animals received selenate, levetiracetam, vehicle subcutaneousinfusion...

10.7554/elife.78877 article EN cc-by eLife 2023-03-09

Temporal lobe epilepsy (TLE) is the most common form of drug resistant epilepsy. Current treatment symptomatic, suppressing seizures, but has no disease modifying effect on epileptogenesis. We examined effects Z944, a potent T-type calcium channel antagonist, as an anti-seizure agent and against progression kindling in amygdala model TLE. The efficacy Z944 (5mg/kg, 10mg/kg, 30mg/kg 100mg/kg) was assessed fully kindled rats (5 class V seizures) compared to vehicle, ethosuximide (ETX,...

10.1371/journal.pone.0130012 article EN cc-by PLoS ONE 2015-08-14

Summary Objective Prolonged electroencephalographic ( EEG ) monitoring in chronic epilepsy rodent models has become an important tool preclinical drug development of new therapies, particular those for antiepileptogenesis, disease modification, and treating drug‐resistant epilepsy. We have developed easy‐to‐use, reliable, computational automated detection electrographic seizures from prolonged recordings Methods applied a novel method based on advanced time‐frequency analysis that detects...

10.1111/epi.14691 article EN Epilepsia 2019-03-13

A history of mild traumatic brain injury (mTBI) is linked to a number chronic neurological conditions, however there still much unknown about the underlying mechanisms. To provide new insights, this study used clinically relevant model repeated mTBI in rats characterize acute and neuropathological neurobehavioral consequences these injuries. Rats were given four sham-injuries or mTBIs allocated 7-day 3.5-months post-injury recovery groups. Behavioral analysis assessed sensorimotor function,...

10.1016/j.nbd.2020.105151 article EN cc-by-nc-nd Neurobiology of Disease 2020-10-27

Abstract Traumatic brain injury (TBI) presents a major global health concern, characterized by variety of negative long term neurological outcomes. Current diagnostic tools lack the sensitivity to fully capture complex pathophysiology TBI and predict long-term consequences, underscoring need for robust methods biomarker detection. This study, conducted within multicenter Epilepsy Bioinformatics Study Antiepileptogenic Therapy (EpiBioS4Rx) framework, used standardized lateral fluid-percussion...

10.1162/imag_a_00471 article EN cc-by Imaging Neuroscience 2025-01-01

Loss of the gene encoding histone acetyltransferase KAT6B (MYST4/MORF/QKF) causes developmental brain abnormalities as well behavioral and cognitive defects in mice. In humans, heterozygous variants cause two disorders, Say-Barber-Biesecker-Young-Simpson syndrome (SBBYSS; OMIM:603736) genitopatellar (GTPTS; OMIM:606170). Although effects homozygous mutations have been documented humans mice, gain-of-function not reported. Here, we show that overexpression Kat6b mice caused aggression,...

10.1016/j.isci.2025.111953 article EN cc-by-nc-nd iScience 2025-02-11

Post-traumatic epilepsy (PTE) is a common, serious, long-term complication of traumatic brain injury (TBI). However, only minority individuals will develop after TBI, and the contribution genetic predisposition to risk acquired warrants further exploration. In this study, we examined whether innate, genetically determined differences in seizure susceptibility between seizure-prone FAST seizure-resistant SLOW rat strains would influence chronic behavioral PTE outcomes experimental TBI. We...

10.1016/j.yebeh.2025.110347 article EN cc-by Epilepsy & Behavior 2025-02-28

Initial studies have found some evidence for transactive response DNA-binding protein 43 (TDP-43) abnormalities after traumatic brain injury (TBI), and the presence of inclusions consisting TDP-43 are a pathological hallmark amyotrophic lateral sclerosis (ALS), condition associated with TBI. However, no study has characterized changes in phosphorylation, mislocalization, fragmentation (i.e., linked to pathology) TBI, how these relate functional outcomes. Further, TBI affects an individual...

10.1089/neu.2017.5491 article EN Journal of Neurotrauma 2018-06-14
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