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WCN19 Journal Invited Speakers V1 JNS-0000116534; No. of Pages 82 ARTICLE IN PRESS Journal of the Neurological Sciences (2019) xxx–xxx Contents lists available at ScienceDirect Journal of the Neurological Sciences journal homepage: www.elsevier.com/locate/jns WCN19 Journal Invited Speakers_V1 WCN19-0547 WCN19-1862 Plenary lecture 1: Fulton award lecture Plenary lecture 2: Neurogenetics Fulton symposium lecture: The battle to beat Parkinson’s disease Neurogenetics P. Brundin F. Alkuraya Van Andel Research Institute, Center for Neurodegenerative Science, King Faisal Specialist Hospital and Research Center, Genetics, Riyadh, Grand Rapids, MI, USA Saudi Arabia While Parkinson’s disease (PD) is classically considered a movement Molecular Precision in Neurology: Contributions by The disorder with much attention paid to the progressive degeneration of Autozygome dopamine neurons in the substantia nigra, research during the past two Clinical genetics and neurology have always worked closely decades have revealed that it is a much more complex disorder. The since neurological presentations are the most frequent phenotypic emerging picture is one of a disorder with a wide variety of non-motor expression of genetic perturbation in humans. “Vulnerability in signs and symptoms and widespread neuropathology involving complexity” applies readily to the complex human nervous system, aggregation of alpha-synuclein (Lewy pathology) in multiple location which is vulnerable to a very wide array of genetic insults. The both in the peripheral and central nervous systems. Furthermore, the evolution of this insight closely follows the evolution of clinical progressive clinical course varies greatly between individuals. Finally, it genetics from karyotype- and single gene-based to the genomics- is apparent that the diagnosis of PD is preceded by a prodromal phase, based field it is currently. Old labels such as developmental delay, encompassing several years, which is coupled to several clinical intellectual disability and cerebral palsy are being refined at an features, e.g. constipation, hyposmia, sleep disorder and depression. unprecedented pace to their individual molecular components Taken together, these findings have provided new clues to the thanks to the widespread application of clinical genomics tools molecular pathogenesis of PD. Some of these clues suggest that that circumvent the human fallibility inherent to the unaided prion-like propagation, neuroinflammation and cellular energy clinical approaches of the past. Despite the massive input from deficits play important roles in the pathogenic process. These outbred populations into this race to deconvolute neurological insights have also spurred the creation of novel and improved disorders molecularly, there remains a considerable gap in our animal models of PD, which hopefully will have greater predictive knowledge of the molecular underpinning of normal neurological validity when assessing experimental therapeutics. development and function that can only be filled by exploring In my presentation, I will discuss several recent studies that have recessive disorders that are exceedingly rare. Consanguineous shed new light on PD pathogenesis, and how they might lead to populations, which are enriched for autozygosity and thus novel therapeutic strategies aimed at slowing disease progression. I the right set up for unmasking the recessiveness of highly will highlight the concepts that different treatments are likely to be informative deleterious alleles, have much to contribute, therefore, effective at different of disease phases (prodromal, early or to molecular precision in neurology as I will highlight in this advanced) and that careful patient selection, minimizing interindi- presentation. vidual variability, will help in the design of effective clinical trials. doi:10.1016/j.jns.2019.10.001 doi:10.1016/j.jns.2019.10.002 0022-510X/$ – see front matter ARTICLE IN PRESS 2 Abstracts / Journal of the Neurological Sciences (2019) xxx–xxx WCN19-0413 The second part of the talk will address how these photoreceptors signal light to the molecular clockwork and by what means this pathway is modified by sleep history. There has been remarkable Plenary lecture 4: The gray zone and brain death progress in understanding the complex intracellular mechanisms that generate circadian rhythms, the molecular pathways whereby Into the grey zone: Detecting covert conscious awareness in the pRGCs entrain circadian biology and sleep has remained poorly behaviourally non-responsive individuals understood. The suprachiasmatic nuclei (SCN) are the site of the primary circadian pacemakers within the mammalian brain. Until A. Owen recently, the model for entrainment involved a simple linear University of Western Ontario, Brain and Mind Institute, London, pathway whereby glutamate release from the pRGCs resulted in Canada Ca2+ influx and raised intracellular cAMP in SCN neurones, which in turn resulted in CREB phosphorylation leading to increased The thought of being ‘locked in’ following a brain injury or aware transcription of two key clock genes, Per1 and Per2.Thissignal during general anaesthesia troubles us all because it awakens the old then advanced or delayed the molecular clockwork. However, an terror of being buried alive. But what does it mean to be awake, but important feature of entrainment is that circadian responses to light entirely unable to respond and what can this tell us about are limited – as typified by jet-lag. Full recovery from jet-lag consciousness itself? In recent years, rapid technological develop- requires a day for every time-zone crossed. We addressed this issue ments in the field of neuroimaging have provided a number of new and have identified and characterized a key role for Salt Inducible methods for revealing thoughts, actions and intentions based solely Kinase 1 (SIK1) and the CREB-regulated transcription co-activator 1 on the pattern of activity that is observed in the brain. I will describe (CRTC1) in clock re-setting. However, our most recent findings have how we are using some of these methods, including functional shown that light entrainment also involves the parallel activation of magnetic resonance imaging (fMRI), electroencephalography (EEG) aCa2+-ERK1/2-AP-1 signalling pathway. Thus both CRE and AP-1 and functional near-infrared spectroscopy (fNIRS), to detect covert regulatory elements drive light-induced clock gene expression. In conscious awareness in patients who are behaviourally entirely non- addition, whilst light activation of the Ca2+-ERK1/2-AP-1 signalling responsive (e.g. vegetative, comatose) and even to allow some of pathway increases Per1 and Per2 expression, sleep/wake behaviour these individuals to communicate their wishes and thoughts. From alters the effects of light on the clock. Our proposed mechanism this perspective, I will contrast those circumstances in which suggests that adenosine acts as a signalling molecule that encodes imaging data can be used to infer awareness in the absence of a wake duration. Adenosine acts via inhibitory A1 receptors on the reliable behavioural response, with those circumstances in which it SCN to inhibit the Ca2+-ERK1/2-AP-1 signalling pathway, which in cannot. This distinction is fundamental for understanding and turn, reduces the expression of Per1 and Per2. Thus sleep/wake interpreting patterns of brain activity in various states of conscious- history, encoded by adenosine, reduces the phase shifting effects of ness (including vegetative state, coma, anaesthesia and sleep), and light upon the circadian system, altering sleep/wake timing. Finally, has profound implications for clinical care, diagnosis, prognosis, the talk will explore how such signalling pathways provide a new ethics and medical-legal decision-making after severe brain injury. It target for the regulation of circadian rhythms and the “pharmaco- also sheds light on more basic scientific questions about how logical” replacement of light for sleep/wake re-setting in individuals consciousness is measured and the neural representation of our lacking eyes or other individuals with severe circadian rhythm own thoughts and intentions. disruption. doi:10.1016/j.jns.2019.10.003 doi:10.1016/j.jns.2019.10.004 WCN19-0373 WCN19-2030 Presidential symposium, WFN medals presentation & soriano Presidential symposium, WFN medals presentation & soriano award plenary lecture award plenary lecture Soriano award lecture: Light, circadian rhythms and sleep: A global role for the world federation of neurology Mechanisms to new therapeutics W.M. Carroll R. Foster Australia University of Oxford, Nuffield Department of Clinical Neurosciences, The Sleep & Circadian Neuroscience Institute SCNi, Oxford, United Kingdom The WFN occupies a unique position in the field of neurology. In the face of increasing need, its challenging mission to foster brain Until recently, it seemed inconceivable to most vision re- health and quality neurology worldwide mandates action. The WFN searchers and ophthalmologists that there could be an is fortunate to be at the centre of the rapid growth in neurosciences unrecognised class of light sensor (photoreceptor) within the eye. and in the increasing awareness of the importance of neuroscience. However, by studying how circadian rhythms and sleep are Further, it has a strengthening organisational structure based on both regulated by the dawn/dusk cycle we demonstrated that there geographical national member societies and disease topic related exists a “3rd class” of photoreceptor within the
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