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Human memory: mathematical models and experiments
I will present my recent work on mathematical modeling of human memory. I will argue that memory recall of random lists of items is governed by the universal algorithm resulting in the analytical relation between the number of items in memory and the number of items that can be successfully recalled. The retention of items in memory on the other hand is not universal and differs for different types of items being remembered, in particular retention curves for words and sketches is different even when sketches are made to only carry information about an object being drawn. I will discuss the putative reasons for these observations and introduce the phenomenological model predicting retention curves.
Mathematical models of neurodegenerative diseases
Neurodegenerative diseases such as Alzheimer’s or Parkinson’s are devastating conditions with poorly understood mechanisms and no cure. Yet, a striking feature of these conditions is the characteristic pattern of invasion throughout the brain, leading to well-codified disease stages associated with various cognitive deficits and pathologies. How can we use mathematical modelling to gain insight into this process and, doing so, gain understanding about how the brain works? In this talk, I will show that by linking new mathematical theories to recent progress in imaging, we can unravel some of the universal features associated with dementia and, more generally, brain functions.
Dr Lindsay reads from "Models of the Mind : How Physics, Engineering and Mathematics Shaped Our Understanding of the Brain" 📖
Though the term has many definitions, computational neuroscience is mainly about applying mathematics to the study of the brain. The brain—a jumble of all different kinds of neurons interconnected in countless ways that somehow produce consciousness—has been described as “the most complex object in the known universe”. Physicists for centuries have turned to mathematics to properly explain some of the most seemingly simple processes in the universe—how objects fall, how water flows, how the planets move. Equations have proved crucial in these endeavors because they capture relationships and make precise predictions possible. How could we expect to understand the most complex object in the universe without turning to mathematics? — The answer is we can’t, and that is why I wrote this book. While I’ve been studying and working in the field for over a decade, most people I encounter have no idea what “computational neuroscience” is or that it even exists. Yet a desire to understand how the brain works is a common and very human interest. I wrote this book to let people in on the ways in which the brain will ultimately be understood: through mathematical and computational theories. — At the same time, I know that both mathematics and brain science are on their own intimidating topics to the average reader and may seem downright prohibitory when put together. That is why I’ve avoided (many) equations in the book and focused instead on the driving reasons why scientists have turned to mathematical modeling, what these models have taught us about the brain, and how some surprising interactions between biologists, physicists, mathematicians, and engineers over centuries have laid the groundwork for the future of neuroscience. — Each chapter of Models of the Mind covers a separate topic in neuroscience, starting from individual neurons themselves and building up to the different populations of neurons and brain regions that support memory, vision, movement and more. These chapters document the history of how mathematics has woven its way into biology and the exciting advances this collaboration has in store.
Deciphering the Dynamics of the Unconscious Brain Under General Anesthesia
General anesthesia is a drug-induced, reversible condition comprised of five behavioral states: unconsciousness, amnesia (loss of memory), antinociception (loss of pain sensation), akinesia (immobility), and hemodynamic stability with control of the stress response. Our work shows that a primary mechanism through which anesthetics create these altered states of arousal is by initiating and maintaining highly structured oscillations. These oscillations impair communication among brain regions. We illustrate this effect by presenting findings from our human studies of general anesthesia using high-density EEG recordings and intracranial recordings. These studies have allowed us to give a detailed characterization of the neurophysiology of loss and recovery of consciousness due to propofol. We show how these dynamics change systematically with different anesthetic classes and with age. As a consequence, we have developed a principled, neuroscience-based paradigm for using the EEG to monitor the brain states of patients receiving general anesthesia. We demonstrate that the state of general anesthesia can be rapidly reversed by activating specific brain circuits. Finally, we demonstrate that the state of general anesthesia can be controlled using closed loop feedback control systems. The success of our research has depended critically on tight coupling of experiments, signal processing research and mathematical modeling.
How to simulate and analyze drift-diffusion models of timing and decision making
My talk will discuss the use of some of these four, simple Matlab functions to simulate models of timing, and to fit models to empirical data. Feel free to examine the code and the relatively brief book chapter that explains the code before the talk if you would like to learn more about computational/mathematical modeling.
Building a synthetic cell: Understanding the clock design and function
Clock networks containing the same central architectures may vary drastically in their potential to oscillate, raising the question of what controls robustness, one of the essential functions of an oscillator. We computationally generate an atlas of oscillators and found that, while core topologies are critical for oscillations, local structures substantially modulate the degree of robustness. Strikingly, two local structures, incoherent and coherent inputs, can modify a core topology to promote and attenuate its robustness, additively. The findings underscore the importance of local modifications to the performance of the whole network. It may explain why auxiliary structures not required for oscillations are evolutionary conserved. We also extend this computational framework to search hidden network motifs for other clock functions, such as tunability that relates to the capabilities of a clock to adjust timing to external cues. Experimentally, we developed an artificial cell system in water-in-oil microemulsions, within which we reconstitute mitotic cell cycles that can perform self-sustained oscillations for 30 to 40 cycles over multiple days. The oscillation profiles, such as period, amplitude, and shape, can be quantitatively varied with the concentrations of clock regulators, energy levels, droplet sizes, and circuit design. Such innate flexibility makes it crucial to studying clock functions of tunability and stochasticity at the single-cell level. Combined with a pressure-driven multi-channel tuning setup and long-term time-lapse fluorescence microscopy, this system enables a high-throughput exploration in multi-dimension continuous parameter space and single-cell analysis of the clock dynamics and functions. We integrate this experimental platform with mathematical modeling to elucidate the topology-function relation of biological clocks. With FRET and optogenetics, we also investigate spatiotemporal cell-cycle dynamics in both homogeneous and heterogeneous microenvironments by reconstructing subcellular compartments.