Controlling Alzheimer's Disease Through the Deep Brain Stimulation to Thalamic Relay Cells.

Xiaoli Yang,Zhongkui Sun,Ruixi Zhang,Jürgen Kurths

doi:10.3389/fncom.2021.636770

Abstract

Experimental and clinical studies have shown that the technique of deep brain stimulation (DBS) plays a potential role in the regulation of Alzheimer’s disease (AD), yet it still desires for ongoing studies including clinical trials, theoretical approach and action mechanism. In this work, we develop a modified thalamo-cortico-thalamic (TCT) model associated with AD to explore the therapeutic effects of DBS on AD from the perspective of neurocomputation. First, the neuropathological state of AD resulting from synapse loss is mimicked by decreasing the synaptic connectivity strength from the Inter-Neurons (IN) neuron population to the Thalamic Relay Cells (TRC) neuron population. Under such AD condition, a specific deep brain stimulation voltage is then implanted into the neural nucleus of TRC in this TCT model. The symptom of AD is found significantly relieved by means of power spectrum analysis and nonlinear dynamical analysis. Furthermore, the therapeutic effects of DBS on AD are systematically examined in different parameter space of DBS. The results demonstrate that the controlling effect of DBS on AD can be efficient by appropriately tuning the key parameters of DBS including amplitude A, period P and duration D. This work highlights the critical role of thalamus stimulation for brain disease, and provides a theoretical basis for future experimental and clinical studies in treating AD.

Highlights

Alzheimer’s disease (AD), a common degenerative disease of the central neural system, is clinically characterized by language disorders, cognitive dysfunction and behavior changes
Based on a modified TCT model containing the nucleus of thalamus and cortex, this work aims to investigate the control effects of deep brain stimulation (DBS) on AD by introducing a DBS voltage to the Thalamic Relay Cells (TRC) neuron population in view of neurocomputation
The neuropathological condition of AD induced by synapse loss is firstly simulated by decreasing one synapse strengthCtsi from the IN neuron population to the TRC neuron population

Summary

Introduction

Alzheimer’s disease (AD), a common degenerative disease of the central neural system, is clinically characterized by language disorders, cognitive dysfunction and behavior changes. The onset of this dynamic disease is relatively slow and difficult to detect. Neurons involved in thinking, learning, memory and movement are damaged, resulting in a memory impairment and even a loss of daily behavior. There have been about 44 million people worldwide suffering from AD or related dementia in 2015. It is estimated that 4.6 million people will have dementia each year and the number will double by 2030 (Prince et al, 2013). The rapid increase of AD patients has brought a heavy burden on families and society, which motivates more and more scientists and physicians to explore more the pathogenesis, diagnosis and treatment of AD

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