Controlling Alzheimer’s Disease Through the Deep Brain Stimulation to Thalamic Relay Cells
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 develo...
Guardado en:
| Autores principales: | , , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Frontiers Media S.A.
2021
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/edb86f71e9e34624af20057c1c761613 |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| Sumario: | 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. |
|---|