Research On The Propagation Model Of Neurodegenerative Disease Protein Based On Magnetic Resonance Imaging

The influence of brain network organization on the process and performance of neurodegenerative diseases is becoming more and more obvious.Parkinsons disease is characterized by atrophy gradually spreading from the midbrain to subcortical structures,and finally reaching the cerebral cortex.Recent studies have shown that the process of neurodegeneration includes the misfolding of endogenous proteins and the transmission of these disease-causing proteins through axons like prions.However,until recently,there is still no definitive conclusion about the transmission process of Parkinsons disease,so this article aims to establish a n effective model to simulate the transmission mode of synuclein.This paper introduces the regulation of Leucine-Rich Repeat Kinase 2(LRRK2)gene on the basis of previous research models,and establishes a transmission model of α-synuclein that integrates structural connection and gene expression—susceptibility-infection-removal model,using LRRK2 gene to reveal the infection and transmission mechanism of pathogenic proteins in the human brain.In this paper,by fusing three brain area maps,a left brain area map containing 42 brain areas is obtained,and using discrete weighted imaging and structural images of 203 individuals in the Human Connectivity Project to trace the brain network of normal people and construct a structural connectivity matrix reflecting the structural connections of the left brain of the human brain.This article normalizes the transcription maps of the three genes in the Allen Brain Atlas,and emphasizes the influence of gene expression on the propagation of synuclein.In this thesis,the empirical atrophy space pattern of Parkinsons disease was obtained through deformation-based morphological measurement on the T1 images of 114 normal people and 234 Parkinsons disease patients proposed by Parkinsons Progression Marking Initiative.In this paper,the model based on LRRK2 gene regulation simulates the loss of neurons in Parkinson’s disease,and the Pearson correlation coefficient between it and the empirical atrophy space pattern reaches 0.73,which is much higher than the classic model(r=0.6),which illustrates the validity of the computational model based on LRRK2 gene regulation in this paper.This paper uses the stable point of the phase trajectory analysis model to theoretically prove the rationality of the newly proposed model.At the same time,this thesis uses two models to fit the empirical spatial atrophy pattern extracted from the MRI data of 155 cases of Xuanwu Hospital.The fitting results of the new model are significantly better than the classic model,reflecting the robustness of the LRRK2 gene regulation model.Finally,according to the two aspects of the lowest transmission threshold of the substantia nigra and the highest relative atrophy,the model based on LRRK2 gene regulation is simulated and verified,and it is verified that the substantia nigra is more likely to be the center of disease transmission.The pathogenic protein transmission model regulated by the LRRK2 gene established in this thesis theoretically reveals that the LRRK2 gene is involved in the infection and transmission mechanism of the pathogenic protein.Compared with the newly proposed model,it can simulate the unique spatial atrophy mode of Parkinson’s disease more effectively.The simulation verifies that the substantia nigra is more likely to be the transmission center of Parkinson’s disease,and it points to new research on the transmission mechanism of Parkinson’s disease.