Julie K. Andersen, Ph.D.
Professor
Buck Institute for Research on Aging
Development of Mitophagy-inducing Small Molecules as Therapeutics for Aging and Alzheimer’s Disease
Alzheimer’s disease (AD) is the leading cause of dementia in those over the age of 65. An underlying process believed to contribute to subsequent neuropathology is loss in mitochondrial function, normally maintained by clearance of defective mitochondria via mitophagy. The small molecule urolithin A (UA) has been demonstrated by several labs, including our own, to be neuroprotective in a variety of mouse AD models. As part of an independent small molecule screen carried out by the lab, we identified a second structurally-related compound we named ‘mitophagy inducing compound’ or MIC. Using C. elegans as an initial validation tool, we showed that both compounds significantly improve mitochondrial function, protect against neuronal cell loss in disease models, and extend lifespan of wildtype animals. These protective effects were found to be translatable to both in vitro and in vivo mammalian models. Recent studies have led to identification of potential drug targets which may serve as novel therapeutic avenues for the disorder. These studies may have important implications for understanding signaling events elicited by these compounds driving their disease-modulating effects.
Mohamed Farah, Ph.D.
Associate Professor in Neurology & Neuroscience
Johns Hopkins University School of Medicine
Degeneration and Regeneration of hiPSC-Derived Peripheral Axons
Axonal dysfunction and degeneration are major early pathological features of neurodegenerative diseases. The focal deformations of axons to form spheroids and swellings, generally referred to as “beads on a string”, are the precursors to axonal fragmentation and degeneration. We investigate early axonal degeneration of human induced pluripotent stem cell (iPSC)-derived motor neurons. Toward this, we have developed a three-dimensional (3D) platform where axonal pathologies can be reliably and reproducibly investigated over time, and have identified a set of differentially expressed axonal mRNAs as intervention targets.
In a second line of research, we are studying peripheral axon regeneration. Peripheral axons have substantial plasticity to regenerate after injury in rodent models. However, human axonal regrowth is very slow, and in most cases, does not result in sufficient functional recovery in disorders of peripheral nerves. While investigating axonal regeneration of iPSC-derived motor neurons, we identified a mutant line that exhibits accelerated rate of axonal regeneration compared to isogenic control. To interrogate molecules responsible for this accelerated rate of outgrowth, we profiled and analyzed RNA expression of axons and cell bodies from mutant and control lines, and identified differentially-expressed genes as prime candidates that we are currently investigating.
Anna Hudson, Ph.D.
Senior Research Fellow
College of Medicine and Public Health
Flinders University
Neural Control of the Human Respiratory Muscles
Jose Parraca, Ph.D.
Professor
Department of Sport and Health
University of Evora
Symptoms and Brain Aging in Fibromyalgia
Fibromyalgia (FM) is a chronic condition characterized by widespread pain, fatigue, sleep disturbances, and cognitive dysfunction, commonly referred to as “fibro fog.” Emerging evidence suggests that FM may be associated with accelerated brain aging, potentially due to neuroinflammatory processes, alterations in neurotransmitter systems, and structural and functional brain changes. Neuroimaging studies indicate a reduction in gray matter volume, altered connectivity in pain-processing networks, and impaired neuroplasticity, which may contribute to symptom severity. Additionally, chronic pain and associated stress in FM could exacerbate age-related cognitive decline and neurodegeneration. Understanding the intersection between FM symptoms and brain aging is crucial for developing targeted interventions to mitigate cognitive impairment and improve the quality of life in affected individuals. This review explores the neurobiological mechanisms linking FM to brain aging and discusses potential therapeutic strategies, including neuromodulation, cognitive training, and non-pharmacological approaches.
Camila Vorkapic, Ph.D.
Associate Professor
Department of Medicine
Universidade Tiradentes
Neuroscience and Mental Health: Protocols for Well-being
The search for well-being is a constant in human life and neuroscience has opened new ways to achieve this condition. During the talk Neuroscience and mental health: protocols for well-being, I will provide a revolutionary view on how we can improve life quality and well being through easy and science-based protocols.
Introduction/Background: The human brain is complex, but it is far from perfect: we cannot regulate our emotions well, we prefer instant gratification, we suffer from relationships, we feel depression and anxiety and we prefer drugs to changing behavior. Are we condemned to not feeling well throughout our lives? Can our brains really change? Viewing the brain as a machine blinds us to the physical realities of mental functions and how we can improve them. We ignore that the brain is a product of evolution, the chemical nature of everything we do, how happiness is a habit and how simple practices can change our mental state. This talk is not just about what the brain is, but mainly about how this self-knowledge can improve our quality of life. In addition to fascinating descriptions of how the brain works, in this talk, you will learn scientifically proven strategies for reshaping your brain and behavior, and experiencing greater well-being.
Monika Wiech , Ph.D.
Assistant Professor
Gdansk University of Physical Education and Sport
Changes in Mood State After Single Health-Related Training Session Depending on the Space and Environment in the Elderly