Analysis of the neural mechanism of spectra decrease in MCI by a thalamo-cortical coupled neural mass model

Objective. In order to deeply understand the neurophysiological mechanism of the spectra decrease in mild cognitive impairment (MCI), this paper studies a new neural mass model, which can simulate various intracerebral electrophysiological activities. Approach. In this study, a thalamo-cortical coupled neural mass model (TCC-NMM) is proposed. The influences of the coupling coefficients and other key parameters on the model spectra are simulated. Then, the unscented Kalman filter (UKF) algorithm is used to reversely identify the parameters in the TCC-NMM. Furthermore, the TCC-NMM and UKF are combined to analyze the spectra reduction mechanism of electroencephalogram (EEG) signals in MCI patients. The independent sample t-test is carried out to statistical analyze the differences of the identified parameters between MCI and normal controls. The Pearson correlation analysis is used to analyze the intrinsic relationship between parameters and the scores of the comprehensive competence assessment scale. Main results. The simulation results show that the decreased cortical synaptic connectivity constants C 1 can result in spectra decrease of the TCC-NMM outputs. The real EEG analysis results show that the identified values of parameter C 1 are significant lower in the MCI group than in control group in frontal and occipital areas and the parameters C 1 are positively correlated with the Montreal Cognitive Assessment (MoCA) scores in the two areas. This consistency suggests that the cortical synaptic connectivity loss from pyramidal cells to excitatory interneurons (eIN) may be one of the neural mechanisms of EEG spectra decrease in MCI. Significance. (a) In this study, a new mathematical model TCCNMM based on anatomy and neurophysiology is proposed. (b) All key parameters in TCC-NMM are studied in detail through the forward and reverse analysis and the influence of these parameters on the output spectra of the model is pointed out. (c) The possible neural mechanism of the decreased spectra in MCI patients is pointed out by the joint analysis of simulation in forward with TCC-NMM and analysis of the actual EEG signals in reverse with UKF identification algorithm. (d) We find that the identified parameter C1 of MCI patients is significantly lower than that of the control group, which is consistent with the simulation analysis of TCC-NMM. So, we suggest that the decreased MCI alpha power spectrum is likely related to the cortical synaptic connection loss from pyramidal cells to eIN.