ArticleFrontiers in computational neuroscience2014
Electrostimulation to reduce synaptic scaling driven progression of Alzheimer's disease.
Article in Frontiers in computational neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Altered synaptic plasticity at hippocampal CA1-CA3 synapses in Alzheimer's disease: integration of amyloid precursor protein intracellular domain and amyloid beta effects into computational models.Frontiers in computational neuroscience · 2023Article
- Training spiking neuronal networks to perform motor control using reinforcement and evolutionary learning.Frontiers in computational neuroscience · 2022Article
- Training a spiking neuronal network model of visual-motor cortex to play a virtual racket-ball game using reinforcement learning.PloS one · 2022Article
- Modeling Neurotransmission: Computational Tools to Investigate Neurological Disorders.International journal of molecular sciences · 2021Review
- Bridging Scales in Alzheimer's Disease: Biological Framework for Brain Simulation With The Virtual Brain.Frontiers in neuroinformatics · 2021Review
- Dysregulation of excitatory neural firing replicates physiological and functional changes in aging visual cortex.PLoS computational biology · 2021Article
- In silico hippocampal modeling for multi-target pharmacotherapy in schizophrenia.NPJ schizophrenia · 2020Article
- The Human Body as a Super Network: Digital Methods to Analyze the Propagation of Aging.Frontiers in aging neuroscience · 2020Article
- Article
- The Impact of Mathematical Modeling in Understanding the Mechanisms Underlying Neurodegeneration: Evolving Dimensions and Future Directions.CPT: pharmacometrics & systems pharmacology · 2017Review
- Trigeminal, Visceral and Vestibular Inputs May Improve Cognitive Functions by Acting through the Locus Coeruleus and the Ascending Reticular Activating System: A New Hypothesis.Frontiers in neuroanatomy · 2017Review
- Article
- Genetic variants in Alzheimer disease - molecular and brain network approaches.Nature reviews. Neurology · 2016Review
- Restoring Behavior via Inverse Neurocontroller in a Lesioned Cortical Spiking Model Driving a Virtual Arm.Frontiers in neuroscience · 2016Article
- Capturing intracellular CaDrug discovery today. Disease models · 2016Article
- Neuronal calcium wave propagation varies with changes in endoplasmic reticulum parameters: a computer model.Neural computation · 2015Article
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Authors and funding
3 authors.
Funding
Abstract
Cell death and synapse dysfunction are two likely causes of cognitive decline in AD. As cells die and synapses lose their drive, remaining cells suffer an initial decrease in activity. Neuronal homeostatic synaptic scaling then provides a feedback mechanism to restore activity. This homeostatic mechanism is believed to sense levels of activity-dependent cytosolic calcium within the cell and to adjust neuronal firing activity by increasing the density of AMPA synapses at remaining synapses to achieve balance. The scaling mechanism increases the firing rates of remaining cells in the network to compensate for decreases in network activity. However, this effect can itself become a pathology, as it produces increased imbalance between excitatory and inhibitory circuits, leading to greater susceptibility to further cell loss via calcium-mediated excitotoxicity. Here, we present a mechanistic explanation of how directed brain stimulation might be expected to slow AD progression based on computational simulations in a 470-neuron biomimetic model of a neocortical column. The simulations demonstrate that the addition of low-intensity electrostimulation (neuroprosthesis) to a network undergoing AD-like cell death can raise global activity and break this homeostatic-excitotoxic cascade. The increase in activity within the remaining cells in the column results in lower scaling-driven AMPAR upregulation, reduced imbalances in excitatory and inhibitory circuits, and lower susceptibility to ongoing damage.
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