Please find our guests for this series by alphabetic order by surname
Much of Dario’s current work is focused on deciphering how autosomal dominant missense mutations that hyper-activate the LRRK2 protein kinase, predispose humans to Parkinson’s disease.
Gary’s research group, the CogGene group has strong collaborative ties with both the neuropsychiatric research group at TCD (with Prof. Aiden Covin & Prof Michael Gill) and the clinical neuroimaging group at NUIG (with Prof Colm McDonald and Dr. Dara Canon). The group studies how brain structure and function are affected by genetic risk factors for psychosis using neuropsychology, MRI and EEG.
Dr. Flanagan is an Assistant Professor in the Addiction Sciences Division of the Department of Psychiatry and Behavioral Sciences. She received a B.A. in psychology at the University of Vermont in 2003 and an M.A. and Ph.D. in clinical psychology at the University of Tennessee 2011. She completed her clinical psychology internship training at the Seattle VA and a NIDA-funded postdoctoral fellowship at the Yale University School of Medicine.
The long-term aim is to understand the fundamental mechanisms of behaviour and how these mechanisms are involved in brain disease.
The research has focussed on the study of genes and proteins that control the synapses between nerve cells. Multiprotein machines comprising many different protein components are responsible for basic innate and learned behaviours and dysfunction in many brain diseases.
Recent work shows that these mechanisms are conserved between mice and humans opening new avenues for diagnosis and therapeutic discoveries. The Genes to Cognition programme has generated a large amount of data and tools that are freely available.
My research interests are in the genetic analysis of disease. Historically, we have worked on the genetic analysis of Alzheimer’s disease and other dementias. More recently, we have worked on Parkinson’s disease and other movement disorders and, most recently on motor neuron disease. Our early studies were on mendelian forms of disease and these studies continue, but an increasing focus has been on the genetic analysis of complex traits related to disease. Additionally, this latter analysis has made us increasingly interested in population genetics because the risk variants for human traits are likely to be different in different racial groups.
The Jasanoff laboratory is developing a new generation of functional magnetic resonance imaging (fMRI) methods to study the neural mechanisms of behavior. Its principal focus is on the design and application of new contrast agents that may help define spatiotemporal patterns of neural activity with far better precision and resolution than current techniques allow. Experiments using the new agents will combine the specificity of cellular neuroimaging with the whole brain coverage and noninvasiveness of conventional fMRI. Introduction of these technologies will have far-reaching consequences in neuroscience, because the new imaging methods will be applicable to studies of any neural system in vivo. The Lab’s goal is to use the methods to build explanatory models of neural network function in animals, with current emphasis on brain circuitry involved in instrumental learning behaviour.
My research focusses on the neurochemical control of behaviour, particularly that involved in psychosis, schizophrenia and addiction. Through the investigation of developing dopamine pathways in experimental animal models my work aims to understand the abnormal circuitry in human neuropsychiatric disorders. Animal models provide an avenue to explore function and neurodevelopment using techniques that cannot be used in human subjects. However, interacting directly with clinicians and performing translational studies are key to putting these facts into context. I work closely with clinical researchers focussed on the daunting task of understanding, identifying and treating early psychosis. This cross-disciplinary research collaboration continues to pursue better outcomes for people suffering from mental illness.
Long-lasting activity-dependent changes in the efficacy of synaptic transmission plays an important role in the development of neural circuits and may mediate many forms of learning and memory. Work from my laboratory over the last 10 years has demonstrated that there is a variety of related but mechanistically distinct forms of synaptic plasticity. A major goal of my laboratory is to elucidate both the specific molecular events that are responsible for the triggering of these various forms of synaptic plasticity and the exact modifications in synaptic proteins that are responsible for the observed, long-lasting changes in synaptic efficacy.
Our data indicates that mitochondria may serve as organizers of local compartments of energy within dendrites. Recent technological advances give us unprecedented ways to study and manipulate mitochondria within individual cell-types and subcellular compartments.
The overarching goal of our research group is to dissect mitochondrial function and its optimization in neuronal compartments. We focus on the proteins that comprise and regulate mitochondria and the other energy supplies such as glycolysis and glial-neuronal networks in different neuronal compartments. We utilize state-of-the-art imaging, advanced proteomics and translatomics technology. We plan to apply our findings to disease model systems for Parkinson’s and ALS where the underlying causes of mitochondrial protein dysfunction are mostly unknown.
The focus of this lab is the study of the molecular basis of synaptic transmission in the mammalian brain. Our primary interests lie in understanding the regulation of vesicle traffic in presynaptic terminals, and how this traffic impacts presynaptic function. Synaptic terminals are specialized cellular structures that carry out carefully orchestrated vesicle trafficking through the interplay of molecular machines. Modulation of synaptic function almost certainly relies on changing the efficiency of one of many of these trafficking steps. Similarly, synaptic dysfunction could easily arise from loss of proper regulation of these steps. We use biophysical tools to characterize the molecular machinery as it functions in living synapses, ultimately always asking the question of how synapses work. We use many types of optical assays in combination with molecular, genetic and chemical tools to determine the molecular basis of various steps of the vesicle cycle as well as the roles of specific proteins that are enriched in the presynaptic terminal. In recent years we have been addressing how endocytosis is regulated at nerve terminals as well as how vesicles are clustered and mobilized for secretion upon action potential firing. The lab continuously develops new assays and approaches to address these questions. Through these studies, we hope to gain insight into how information is controlled at the synaptic level in both normal and diseased states of brain function.