This lesson is a general overview of overarching concepts in neuroinformatics research, with a particular focus on clinical approaches to defining, measuring, studying, diagnosing, and treating various brain disorders. Also described are the complex, multi-level nature of brain disorders and the data associated with them, from genes and individual cells up to cortical microcircuits and whole-brain network dynamics. Given the heterogeneity of brain disorders and their underlying mechanisms, this lesson lays out a case for multiscale neuroscience data integration.
The state of the field regarding the diagnosis and treatment of major depressive disorder (MDD) is discussed. Current challenges and opportunities facing the research and clinical communities are outlined, including appropriate quantitative and qualitative analyses of the heterogeneity of biological, social, and psychiatric factors which may contribute to MDD.
This is the first of two workshops on reproducibility in science, during which participants are introduced to concepts of FAIR and open science. After discussing the definition of and need for FAIR science, participants are walked through tutorials on installing and using Github and Docker, the powerful, open-source tools for versioning and publishing code and software, respectively.
This lesson contains both a lecture and a tutorial component. The lecture (0:00-20:03 of YouTube video) discusses both the need for intersectional approaches in healthcare as well as the impact of neglecting intersectionality in patient populations. The lecture is followed by a practical tutorial in both Python and R on how to assess intersectional bias in datasets. Links to relevant code and data are found below.
This lesson delves into the opportunities and challenges of telepsychiatry. While novel digital approaches to clinical research and care have the potential to improve and accelerate patient outcomes, researchers and care providers must consider new population factors, such as digital disparity.
This lesson explains the fundamental principles of neuronal communication, such as neuronal spiking, membrane potentials, and cellular excitability, and how these electrophysiological features of the brain may be modelled and simulated digitally.
This is a continuation of the talk on the cellular mechanisms of neuronal communication, this time at the level of brain microcircuits and associated global signals like those measureable by electroencephalography (EEG). This lecture also discusses EEG biomarkers in mental health disorders, and how those cortical signatures may be simulated digitally.
This lesson describes the principles underlying functional magnetic resonance imaging (fMRI), diffusion-weighted imaging (DWI), tractography, and parcellation. These tools and concepts are explained in a broader context of neural connectivity and mental health.
This lecture covers the emergence of cognitive science after the Second World War as an interdisciplinary field for studying the mind, with influences from anthropology, cybernetics, and artificial intelligence.
This lesson characterizes different types of learning in a neuroscientific and cellular context, and various models employed by researchers to investigate the mechanisms involved.
This lesson describes spike timing-dependent plasticity (STDP), a biological process that adjusts the strength of connections between neurons in the brain, and how one can implement or mimic this process in a computational model. You will also find links for practical exercises at the bottom of this page.
This lesson discusses a gripping neuroscientific question: why have neurons developed the discrete action potential, or spike, as a principle method of communication?
This lecture focuses on how the immune system can target and attack the nervous system to produce autoimmune responses that may result in diseases such as multiple sclerosis, neuromyelitis, and lupus cerebritis manifested by motor, sensory, and cognitive impairments. Despite the fact that the brain is an immune-privileged site, autoreactive lymphocytes producing proinflammatory cytokines can cause active brain inflammation, leading to myelin and axonal loss.