Our laboratory integrates molecular, imaging, electrophysiological and neurobehavioural approaches to examine the pathophysiology and treatment of central nervous system injury, using spinal cord injury as a model system. Current studies in SCI are focused on understanding the mechanisms of the secondary injury after SCI with a focus on examining the role of inflammation, development of novel neuroprotective strategies and the use of stem cell transplantation strategies to repair the spinal cord. Our publications include ones that were the first used to describe secondary spinal cord injury mechanisms, first to use Rilozole to improve functional spinal recovery, first to term Degenerative Cervical Myelopathy. To read about more of our ground breaking research - visit our website.
The Hodaie lab focuses primarily on structural MRI imaging in functional neurosurgery with a special interest in neuropathic pain. We have also published key papers in the area focusing on methods of small fiber tractography and structural neuroanatomical changes in the central nervous system (CNS) gray and white matter in facial neuropathic pain. Much of our research focuses on trigeminal neuralgia, an extremely painful neuropathic pain relating to disturbances and complications with a branch of the trigeminal nerve, a nerve providing sensation to many parts of the face. To learn more about our research and projects, visit our website.
Research at the Kongkham lab is focused on the genomics and epigenetics of primary and metastatic adult brain tumors. Our research efforts are on the genetics and biology of human glioblastoma multiforme. The research will be focused on the study of epigenetic factors involved in the pathogenesis of primary glial tumours as well as CNS metastatic disease. Our research laboratory is within the Arthur and Sonia Labatt Brain Tumour Research Centre at The Hospital for Sick Children. To learn more about our work, check out some publications using this link.
Poor handling and elimination of misfolded proteins has been identified as central in the molecular pathogenesis of Parkinson’s disease (PD) . A special class of proteins within the cell called “chaperones” is responsible for refolding misfolded or damaged proteins and if they cannot adequately deal with these misfolded proteins, they are targeted to specialized disposal systems. Together these pathways are critical to maintain protein quality control within a cell. If they are dysfunctional or overwhelmed then neurodegeneration ensues. Our ultimate goal is to find ways to mitigate the loss of neurons in the brain to be able to slow or even halt the progression of PD and other neurodegenerative disorders. To learn more about our projects and publications, visit my UHN Research profile.
We do laboratory work involving cell death in Parkinson's disease, effects of stimulation on hippocampal neurogenesis and animal models of deep brain stimulation. We look to examine neurons and brain circuits involved in neurological disorders like Parkinson's and depression. We then also explore treatments for these disorders. Deep brain stimulation has been proven to relieve some symptoms of Parkinson's disease and is showing promise in being a treatment for depression. Look through our publications to learn more about our research.
Our research at the Radovanovic lab focuses on the surgical management of ruptured and unruptured aneurysms, arteriovenous malformations (AVMs) and dural arteriovenous fistulae, using minimally invasive techniques such as supraorbital and lateral supraorbital craniotomies. It also examines the developmental signaling and genetics of cerebral arteriovenous malformations and brain tumours. To learn more about our work, check out some publications.
In the field of experimental spinal cord injury, I have developed several models of acute compression injury of the spinal cord and several quantifiable outcome measures. Various blood flow and angiographic techniques have been used to study post-traumatic ischemia.
I have examined endogenous and transplanted stem/progenitor cells in the spinal cord. A variety of neurotrophic factors and other agents have been examined in rodent spinal cord injury.
We have studied the survival, migration and differentiation of endogenous and transplanted adult rat spinal cord ependymal region stem/progenitor cells generated in vitro from neurospheres. We have shown the effects of trasnplanting these cells in the adult rodent spinal cord. We are also examining a number of bioengineering strategies involving guidance channels and drug delivery systems for axonal regeneration.
Recently, we have accomplished the culturing and transplantation of human adult spinal cord derived stem cells into rats with spinal cord injury. To learn more, explore our publications.
Research in my lab is centered around the cellular and molecular mechanisms of neuronal damage during stroke and other injuries such as epilepsy and trauma.
Our focus is on calcium-regulated signaling pathways that cause neurons to die when injured. Our main contributions to this field has been the determination that acute damage to neurons is mediated by distinct signaling pathways that are specifically associated with certain types of cell membrane receptors and ion channels.
We are working on elucidating these pathways, with the goal of finding rate-limiting steps that might be amenable to modulation by pharmacological or genetic means. The ultimate goal therefore, is to design rational therapeutic strategies for neuronal injury based on a concrete understanding of the molecular mechanisms that cause it.
The scope of our projects includes studies in tissue culture and in-vivo models. Techniques most commonly used are neurophysiological, including Ca2+ imaging, confocal imaging, electrophysiology, molecular biology, and protein chemistry. To learn more, check out some of our publications.
In my lab, called the Neuron to Brain Laboratory, I am interested in electrical oscillations of the brain - both physiological and pathological. I study such oscillations in humans and rodents, both in vivo and in vitro. I am particularly interested in how these oscillations organize activity in the brain, and how cortical microcircuits support such organized activity. We use electrocorticography, local field potential, multielectrode array, and whole cell recordings techniques. We as well use optogenetic techniques to control specific neuronal populations, as we try to elucidate dynamical mechanisms underlying critical state transition like the transition to seizure. A number of computational techniques are employed to characterize activity at the single cell and population level to gain insight to how cellular activity ultimately results in cortical computations, and derangement like those that occur in epilepsy. Visit our website to learn more about this research.
Research interests at the Zadeh lab include genomic and basic science investigations of brain tumours. Most recently I have published a landmark paper in Nature Genetics establishing the genomic landscape of schwannomas and is working on understanding the genomic and molecular regulators of aggressive meningiomas.
Our research laboratory is focused on studying the molecular mechanisms of glioma angiogenesis and molecular regulators of tumour metabolism. Specifically investigating the role of bone marrow derived cells in supporting tumour vasculature in gliomas and how differentiation into macrophage and microglia population plays a role in escape mechanisms of evading anti-angiogenic therapy. A second focus of the laboratory, on tumour metabolism, explores the interplay between altered metabolism in response to anti-angiogenic therapy. I also have a translational program, dedicated to establishing the genomic landscape of menigniomas and schwannomas. The laboratory is funded through peer-reviewed grants from a number of agencies such as CIHR, Terry Fox New Investigator grant, CCSRI, CRS, BrainChild and others. Visit our lab website to learn more.