Thursday, October 19 – 08:00 AM ET

Jerzy Olszewsky Invited Lecture
Dr. John Woulfe, MD PhD

John Woulfe is a Clinical Neuropathologist at The Ottawa Hospital, Associate Professor in the Faculty of Medicine at The University of Ottawa, and Physician Investigator at The Ottawa Hospital Research Institute. He completed his medical degree at McMaster University, his MSc in neuroanatomy at The University of Western Ontario, and his PhD in the Department of Neurology and Neurosurgery at the Montreal Neurological Institute of McGill University. Dr. Woulfe’s research interests are focussed on neurodegenerative diseases and “non-pathological” (or preferably “quasi-pathological”), brain ageing. His fascination with nuclear inclusion bodies and obsession with intranuclear rods has led him on a tortuous journey which has oddly culminated in the study of metabolic enzyme phase separation and filamentation in neurons and how this impacts neuronal function and survival. He has recently established valuable collaborations with other investigators in this fascinating and burgeoning field.

Title: Olszewski, cellular snakes, and the substantia nigra.

Substantia nigra dopaminergic neurons undergo selective degeneration during Parkinson’s disease as well as during normal ageing. The factors underlying the latter are incompletely understood. In this presentation, I will present morphological evidence that phase separation and filamentation of the metabolic enzyme IMPDH in these cells plays an adaptive role in their development but that its aggregation in the nucleus imposes detrimental consequences as they age. This model of antagonistic pleiotropy sheds light on the role of purine metabolism in nigral development and reveals a novel protein aggregation mechanism underlying age-related nigral degeneration.

Learning Objectives:

  1. Understand that substantia nigra neurons are lost during normal aging
  2. Understand that Marinesco bodies and IMPDH nuclear inclusions may contribute to age-related loss of nigral dopamine neurons
  3. Understand the role of filamentation in the regulation of metabolic enzyme activity
  4. Understand the possible role of inosine monophosphate dehydrogenase filamentation and crystallization in the development, survival, and degeneration of the human substantia nigra
COI Disclosure:

None to disclose.

Saturday, October 21 – 08:00 AM CDT

Invited Lecture
Meryem Oskoui, MD

Dr. Maryam Oskoui is Director of Pediatric Neurology at the Montreal Children’s Hospital, McGill University. She is a Senior Clinical Research Scholar of the Fonds de recherche du Québec with a focus in clinical trials in pediatric neuromuscular disorders and Principal investigator for INFORM SMA, a Strategy for Patient Oriented Research, an innovative clinical trial initiative supported by the CIHR. Dr. Oskoui serves as an evidence-based methodologist for the American Academy of Neurology and has contributed to numerous clinical care guidelines.

Title: Epidemiology and clinical aspects of cerebral palsy in Canada

An update on the epidemiology of cerebral palsy will be provided, reviewing the global prevalence across risk groups, predictive models of developing CP in infants, and examining the role of genetic testing in this population.

Learning Objectives:

  1. Compare the prevalence of cerebral palsy across risk groups
  2. Predict the risk of cerebral palsy in infants
  3. Counsel families on the yield of geentic testing i chidlren diagnosed with cerebral palsy
COI Disclosure:

I have a relationship with a for-profit and/or a not-for-profit organization to disclose. 

Funded grants or clinical trials:
Biogen, Rohe, Novartis, Santhera
Description of relationship(s) : Site investigator for clinical trials in pediatric neuromuscular disorders

Saturday, October 21 – 08:50 AM ET

Gordon Mathieson Lecture
Dr. Marc Del Bigio, MD, PhD

Dr. Del Bigio was born in Winnipeg and attended medical school at the University of Manitoba, graduating in 1982 with MD and BSc(Med) degrees. Following a surgical internship, he pursued a PhD degree in the Department of Anatomy, also at the University of Manitoba, graduating in 1987. He began clinical training in neurosurgery, but reevaluated his career goals during a research postdoc at the University of Saskatchewan. He completed training in Neuropathology at the University of Toronto and obtained his FRCPC in 1993. After a postdoctoral research period at the Université de Paris, he was recruited back to the University of Manitoba in 1994. He has worked as a neuropathologist and research scientist in the Department of Pathology since then. His professional diagnostic activities in Neuropathology span the full spectrum of surgical and autopsy material. His particular clinical interests are in pediatric neuropathology (including perinatal injuries and inherited / metabolic disorders) and forensic neuropathology. Research interests include: hydrocephalus, hemorrhagic brain damage, mechanical properties of the brain, effects of substance abuse on the brain (especially alcohol and volatile solvents).

Experiences with the introduction of competency based medical training in Anatomic Pathology

Description to come

Learning Objectives:

1. TBC
2. TBC
3. TBC

COI Disclosure:


Get Presentation

Presentation to come

Title: In utero infections and their effects on the developing brain.

Dr. Del Bigio will discuss how the developing brain is potentially at risk during gestation in the context of maternal infection. There will be no attempt to describe important pathology in other organ systems.

Learning Objectives:

  1. Describe briefly milestones in human brain development in utero
  2. Describe the general mechanisms through which viral infections damage the developing brain
  3. List three examples of in utero brain infections in addition to the classic STORCH spectrum
COI Disclosure:

I have a relationship with a for-profit and/or a not-for-profit organization to disclose.

Direct financial payments including receipt of honoraria:
Cambridge University Press
Description of relationship(s) : book sales royalties (Perinatal Neuropathology)

Saturday, October 21 – 10:00 AM ET

David Robertson Lecture
Dr. David van Essen, PhD

David Van Essen is the Alumni Endowed Professor of Neuroscience at Washington University in St Louis. His laboratory has carried out pioneering studies of the structure, function, connectivity, development, and evolution of cerebral cortex in humans and nonhuman primates, including a human cortical parcellation of unprecedented detail and quality. A major emphasis of his lab is on the development and utilization of methods for computerized brain mapping as well as neuroinformatics tools that facilitate data analysis and data mining. He has a long-standing interest in mechanisms of neural development, particularly on how and why the cerebral cortex gets its folds.

Dr. Van Essen received his undergraduate degree from Caltech and his Ph.D. from Harvard University. He joined the Caltech faculty in 1976 and moved to Washington University in 1992, where he chaired the Department of Anatomy and Neurobiology for two decades. He has served in many leadership positions, including President of the Society of Neuroscience and founding chair of the Organization for Human Brain Mapping. He has received many awards and honors, including the Krieg Cortical Discoverer Award (Cajal Club), the Glass Brain Award (Organization for Human Brain Mapping), the George A. Miller Prize (Cognitive Neuroscience Society), and the Carl and Gerti Cori Faculty Achievement Award (Washington University School of Medicine). He is a fellow of the American Association for the Advancement of Science and a member of the National Academy of Sciences.

Title: Models And Mechanisms Of Cerebral Cortical Expansion And Folding

Morphogenesis of the nervous system involves a complex pattern of physical forces (tension and pressure) acting on cells and tissues that have an intricately organized cytoskeletal infrastructure. This lecture will focus on the phenomena of cortical expansion and folding that take place over an extended period of prenatal and postnatal development. Many complementary mechanisms likely contribute to cortical expansion and folding, some related to regulating cell proliferation and migration and others related to specific types and patterns of mechanical tension and pressure. Three distinct multi-mechanism models will be evaluated in relation to a set of 18 key experimental observations and findings. The Composite Tension Plus (CT+) model includes 10 distinct mechanisms and has the greatest explanatory power among published models to date. However, much needs to be done in order to validate specific mechanistic components and to assess their relative importance in different species.

Learning Objectives:

  1. State two benefits of increased cortical surface area
  2. State two benefits of cortical folding
  3. Identify several distinct models for cortical expansion and folding
  4. Describe strengths and limitations of each model
COI Disclosure:

I have a relationship with a for-profit and/or a not-for-profit organization to disclose.

Direct financial payments including receipt of honoraria:
1) University of California at San Diego;
2) NIH
Description of relationship(s) : Spring and fall (two 2-day meetings, 2022 and 2023: University of California at San Diego. I serve on the External Advisory Board for the NIH-funded Adolescent Brain and Cognitive Development Project (UCSD, lead institution). An honorarium of $500 per meeting was provided ($2,000 in 2022, 2023); 2) February, 2023. I received a $250 honorarium for ad hoc service on a 1-day virtual NIH study section

Membership on advisory boards or speakers’ bureaus:
1) Adolescent Brain and Cognitive Development Project;
2) T. Denny Sanford Institute for Compassion and Empathy
Description of relationship(s) : 1) I am on the external advisory board for the T. Denny Sanford Institute for Compassion and Empathy. I participated in one 1-day virtual meeting in the fall of 2022; 2) I serve on the External Advisory Board for the NIH-funded Adolescent Brain and Cognitive Development Project (UCSD, lead institution) and participate in Spring and fall (two 2-day meetings, 2022 and 2023

Funded grants or clinical trials:
Description of relationship(s) : 1) Connectome Coordination Facility II; 2) Reconstructions and Representations of Cerebral Cortex; 3) Vulnerability and Resiliency in the Aging Adult Brain Connectome (AABC); 4) Functionally guided adult whole brain cell atlas in human and NHP

Saturday, October 21 – 10:50 AM ET

Invited Lecture
Dr. Praveen Ballabh, MD

My research focuses on understanding the cellular and molecular mechanisms of brain injury produced by intraventricular hemorrhage (IVH) in premature infants and developing strategies to restore the development and function of the brain in the survivors with IVH. For these studies, we employ our animal model of glycerol-induced IVH in prematurely delivered rabbit pups. Using this model, we have shown that COX2 inhibition, thyroxine treatment, or degradation of hyaluronan enhance myelination and neurological outcomes in our rabbit model of IVH. Since thyroxine treatment promotes myelination in rabbits with IVH, I have initiated a clinical trial (pilot study) of thyroxine in premature infants with moderate-severe IVH. In the early stage of my career, we studied ganglionic eminence (germinal matrix) of premature human infants and premature rabbits to understand the underlying cause of intrinsic fragility of germinal matrix vasculature. We discovered that there is rapid angiogenesis in the germinal matrix vasculature unlike cortical plate and white matter (Nature Medicine 2007). Moreover, there is a paucity of pericytes and reduced expression of fibronectin in the angiogenic vessels of the germinal matrix (J. Neuroscience 2008), which renders them fragile and vulnerable to hemorrhage. I have recently published on the effect of IVH on glutamatergic neurogenesis and interneuron neurogenesis (Cerebral Cortex 2018, Brain 2022). Together, we perform developmental studies related to the effect of IVH on cerebral germinal matrix, white matter, and gray matter.

Title: Perinatal intraventricular hemorrhage and brain development

While intraventricular hemorrhage (IVH) predominantly damages the periventricular white matter, it induces substantial injury to
the cerebral gray matter. IVH destroys the germinal matrix, suppresses neurogenesis, and disrupts corticogenesis, thereby reducing the number of neurons in the upper cortical layers. The pathogenesis of gray matter injury is attributed to IVH-induced oxidative stress, inflammation, and mass effect damaging the germinal matrix. The occurrence of IVH suppresses both glutamatergic and GABAergic neurogenesis reducing the population of cortical pyramidal neurons and interneurons. Wnt and Shh signaling regulates the production of glutamatergic neurons and interneurons in the telencephalon respectively. Accordingly, targeting these pathways has restored neurogenesis in animal models. Preclinical and clinical studies suggest that removing blood clots from the ventricles and reducing oxidative stress and inflammation improves the outcome of survivors with IVH.

Learning Objectives:

  1. Discuss recent advances in the understanding of the pathogenesis of gray matter injury in premature infants
  2. Identify the emerging therapeutic strategies to reverse the gray matter injuries in infants with IVH
COI Disclosure:

None to disclose.

Saturday, October 21 – 11:40 AM ET

Invited Lecture
Dr. William Foulkes, MBBS, PhD

I am a senior clinician-scientist who has worked in the area of inherited susceptibility to cancer for over 25 years. My research career centers on understanding inherited susceptibility to cancer: for all these years, the direction of my program has been to move from cancer gene mutation discovery to clinical applications. This work is intimately associated with my clinical career, as this process enables us to directly use patients as a source of discovery and to rapidly translate the results of our work for the benefit of patients and their families.

Title: Cns Manifestations Of Dicer1 Tumor Predisposition Syndrome

In this talk I will introduce the microRNA biogenesis protein DICER1 and how it functions in health and in illness. I will then discuss the syndrome, DICER1 tumour predisposition syndrome (DTPS), which is caused by germline pathogenic variants in DICER1. It is associated with a broad range of mainly pediatric and adolescent onset tumors. I will spend most of my time discussing the CNS manifestations of DTPS.

Learning Objectives:

  1. To become acquainted with the basic principles of microRNA biogenesis
  2. To be aware of the protean CNS manifestations of DICER1 perturbation
  3. To learn how DICER1-related sarcomas arising at different anatomical sites share molecular similarities.
COI Disclosure:

None to disclose.