Preventing neurodegenerative memory loss in Hopfield neuronal networks using cerebral organoids or external microelectronics

DOI10.1155/2017/6102494MaRDI QIDQ1664526zbMATH OpenOpenAlexWikidataFDO

Authors Y. Aharonov

Publication date 27 August 2018

Published in Computational \& Mathematical Methods in Medicine (Search for Journal in Brave)

Copyright license Creative Commons Attribution 4.0 International

Full work available at URL https://doi.org/10.1155/2017/6102494

zbMATH Keywords

cerebral organoidsexternal microelectronicsHopfield neuronal networkspeventing neurodegenerative memory loss

Mathematics Subject Classification ID

Neural networks for/in biological studies, artificial life and related topics (92B20) Neural biology (92C20) Medical applications (general) (92C50)

Review text

Summary: Developing technologies have made significant progress towards linking the brain with brain-machine interfaces (BMIs) which have the potential to aid damaged brains to perform their original motor and cognitive functions. We consider the viability of such devices for mitigating the deleterious effects of memory loss that is induced by neurodegenerative diseases and/or traumatic brain injury (TBI). Our computational study considers the widely used Hopfield network, an autoassociative memory model in which neurons converge to a stable state pattern after receiving an input resembling the given memory. In this study, we connect an auxiliary network of neurons, which models the BMI device, to the original Hopfield network and train it to converge to its own auxiliary memory patterns. Injuries to the original Hopfield memory network, induced through neurodegeneration, for instance, can then be analyzed with the goal of evaluating the ability of the BMI to aid in memory retrieval tasks. Dense connectivity between the auxiliary and Hopfield networks is shown to promote robustness of memory retrieval tasks for both optimal and nonoptimal memory sets. Our computations estimate damage levels and parameter ranges for which full or partial memory recovery is achievable, providing a starting point for novel therapeutic strategies.

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Cites work

• Compromised axonal functionality after neurodegeneration, concussion and/or traumatic brain injury
• Neural networks and physical systems with emergent collective computational abilities
• Neurons with graded response have collective computational properties like those of two-state neurons

Cited in

(2)

• Dynamic analysis of synaptic loss and synaptic compensation in the process of associative memory ability decline in Alzheimer's disease
• NMDA receptor alterations after mild traumatic brain injury induce deficits in memory acquisition and recall

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