scholarly journals Teaching Machines to Recognize Neurodynamic Correlates of Team and Team Member Uncertainty

2019 ◽  
Vol 13 (4) ◽  
pp. 310-327 ◽  
Author(s):  
Ronald H. Stevens ◽  
Trysha L. Galloway

We describe efforts to make humans more transparent to machines by focusing on uncertainty, a concept with roots in neuronal populations that scales through social interactions. To be effective team partners, machines will need to learn why uncertainty happens, how it happens, how long it will last, and possible mitigations the machine can supply. Electroencephalography-derived measures of team neurodynamic organization were used to identify times of uncertainty in military, health care, and high school problem-solving teams. A set of neurodynamic sequences was assembled that differed in the magnitudes and durations of uncertainty with the goal of training machines to detect the onset of prolonged periods of high level uncertainty, that is, when a team might require support. Variations in uncertainty onset were identified by classifying the first 70 s of the exemplars using self-organizing maps (SOM), a machine architecture that develops a topology during training that separates closely related from desperate data. Clusters developed during training that distinguished patterns of no uncertainty, low-level and quickly resolved uncertainty, and prolonged high-level uncertainty, creating opportunities for neurodynamic-based systems that can interpret the ebbs and flows in team uncertainty and provide recommendations to the trainer or team in near real time when needed.

1990 ◽  
Author(s):  
James M. Georgoulakis ◽  
Atanacio C. Guillen ◽  
Cherry L. Gaffney ◽  
Sue E. Akins ◽  
David R. Bolling ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Ethan W. Hass ◽  
Zachary A. Sorrentino ◽  
Grace M. Lloyd ◽  
Nikolaus R. McFarland ◽  
Stefan Prokop ◽  
...  

AbstractMultiple system atrophy (MSA) is an insidious middle age-onset neurodegenerative disease that clinically presents with variable degrees of parkinsonism and cerebellar ataxia. The pathological hallmark of MSA is the progressive accumulation of glial cytoplasmic inclusions (GCIs) in oligodendrocytes that are comprised of α-synuclein (αSyn) aberrantly polymerized into fibrils. Experimentally, MSA brain samples display a high level of seeding activity to induce further αSyn aggregation by a prion-like conformational mechanism. Paradoxically, αSyn is predominantly a neuronal brain protein, with only marginal levels expressed in normal or diseased oligodendrocytes, and αSyn inclusions in other neurodegenerative diseases, including Parkinson’s disease and Dementia with Lewy bodies, are primarily found in neurons. Although GCIs are the hallmark of MSA, using a series of new monoclonal antibodies targeting the carboxy-terminal region of αSyn, we demonstrate that neuronal αSyn pathology in MSA patient brains is remarkably abundant in the pontine nuclei and medullary inferior olivary nucleus. This neuronal αSyn pathology has distinct histological properties compared to GCIs, which allows it to remain concealed to many routine detection methods associated with altered biochemical properties of the carboxy-terminal domain of αSyn. We propose that these previously underappreciated sources of aberrant αSyn could serve as a pool of αSyn prion seeds that can initiate and continue to drive the pathogenesis of MSA.


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