This day-long, CME credit-eligible workshop will provide participants with an understanding of the common and distinct features of neurodegenerative diseases, which include not only those affecting the brain, such as Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, vascular dementia, frontotemporal dementia, and mixed dementia; but also the ocular diseases including age-related macular degeneration, glaucoma, diabetic retinopathy, and inherited retinal degenerative diseases. Some questions that will be addressed during this fourth pre-symposium workshop, starting from small (Section 1. Mitochondria In Health and Neurodegeneration; and Section 2. Glucose and Lipid Metabolism) and ending with a more wholistic (Section 3. System-level Energy Dysfunction and Metabolic Disorders) point of view: •Why does the nervous system (including the brain and eyes) have a unique energy demand? •How can one evaluate metabolic fitness? •How can only tiny changes in energy, metabolism and/or mitochondria lead to neurodegenerative disease?•Is there a definite ‘tipping point’ that could be prevented in humans to delay onset of disease?•What role do comorbidities, like diabetes and other insulin/energy/metabolism-dysfunction diseases, play in neurodegenerative diseases?•How can one study this in living humans? •Are there common elements across these diseases that could give a clue to preventions and future treatments?Section 1 Summary: Mitochondria are essential organelles that regulate multiple processes essential for neuronal function including metabolic balance, intracellular calcium homeostasis, production of reactive oxygen species, and apoptotic signaling. Accumulating evidence indicates that mitochondrial defects play a central role in the pathogenesis of neurodegenerative diseases. This session will cover new insights into mitochondrial dynamics, trafficking, transmitophagy, and damage as well as novel therapeutic strategies to increase mitochondrial health in eye and brain diseases.Section 2 Summary: Individual cell-types in the brain have unique energy requirements and unique roles in meeting the energetic demands placed on the brain. Disruption in cellular cross-talk and cell-autonomous energy occur during the setting of neurodegenerative disease. A more refined disruption of the cellular and intercellular metabolic defects will likely offer new insights into neurodegenerative disease and perhaps illuminate novel therapeutic approaches.Section 3 Summary: Metabolic conditions and diabetes are risk factors for both Alzheimer’s disease and eye diseases. In addition to hypoperfusion restricting blood flow, they also impact brain energy metabolism including insulin signaling and glucose utilization. In this section, the speakers will discuss how brain metabolism and insulin signaling are impaired in these neurodegenerative conditions and how these pathways can be targeted for therapy to treat brain and eye diseases, and to promote healthy brain aging.

Supported with an educational grant by BrightFocus