The features analysis of hemoglobin expression on visual information transmission pathway in early stage of Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized primarily by cognitive impairment. The motivation of this paper is to explore the impact of the visual information transmission pathway (V-H pathway) on AD, and the following feature were observed: Hemoglobin expression on the V-H pathway becomes dysregulated as AD occurs so as to the pathway becomes dysfunctional. According to the feature, the following conclusion was proposed: As AD occurs, abnormal tau proteins penetrate bloodstream and arrive at the brain regions of the pathway. Then the tau proteins or other toxic substances attack hemoglobin molecules. Under the attack, hemoglobin expression becomes more dysregulated. The dysfunction of V-H pathway has an impact on early symptoms of AD, such as spatial recognition disorder and face recognition disorder.

An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized primarily by a decline in cognitive function. However, the etiopathogenesis of AD is unclear. N6-methyladenosine (m6A) is abundant in the brain, and it is interesting to explore the relationship between m6A and AD causes. In this paper, the gene expression of METTL3 and NDUFA10 were found to correlate with the Mini-mental State Examination (MMSE), which is a clinical indicator of the degree of dementia. METTL3 is involved in post-transcriptional methylation and the formation of m6A. NDUFA10 encodes the protein with NADH dehydrogenase activity and oxidoreductase activity in the mitochondrial electron transport chain. The following three characteristics were observed in this paper: 1. The lower the expression level of NDUFA10, the smaller the MMSE, and the higher the degree of dementia. 2. If the expression level of METTL3 dropped below its threshold, the patient would have a risk of AD with a probability close to 100%, suggesting a basic necessity for m6A to protect mRNA. 3. The lower the expression levels of both METTL3 and NDUFA10, the more likely the patient would suffer from AD, implying the coherence between METTL3 and NDUFA10. Regarding the above discovery, the following hypothesis is presented: METTL3 expression level is downregulated, then the m6A modification level of NDUFA10 mRNA is also decreased, thereby reducing the expression level of NDUFA10-encoded protein. Furthermore, the abnormal expression of NDUFA10 contributes to the assembly disorder of mitochondrial complex I and affects the process of the electron respiratory chain, with the consequent development of AD. In addition, to confirm the above conclusions, the AI Ant Colony Algorithm was improved to be more suitable for discovering the characteristics of AD data, and the SVM diagnostic model was applied to mine the coherent effects on AD between METTL3 and NDUFA10. In conclusion, our findings suggest that dysregulated m6A leads to altered expression of its target genes, thereby affecting AD's development.

The coherence between PSMC6 and α-ring in the 26S proteasome is associated with Alzheimer's disease.

Alzheimer's disease (AD) is a heterogeneous age-dependent neurodegenerative disorder. Its hallmarks involve abnormal proteostasis, which triggers proteotoxicity and induces neuronal dysfunction. The 26S proteasome is an ATP-dependent proteolytic nanomachine of the ubiquitin-proteasome system (UPS) and contributes to eliminating these abnormal proteins. This study focused on the relationship between proteasome and AD, the hub genes of proteasome, PSMC6, and 7 genes of α-ring, are selected as targets to study. The following three characteristics were observed: 1. The total number of proteasomes decreased with AD progression because the proteotoxicity damaged the expression of proteasome proteins, as evidenced by the downregulation of hub genes. 2. The existing proteasomes exhibit increased activity and efficiency to counterbalance the decline in total proteasome numbers, as evidenced by enhanced global coordination and reduced systemic disorder of proteasomal subunits as AD advances. 3. The synergy of PSMC6 and α-ring subunits is associated with AD. Synergistic downregulation of PSMC6 and α-ring subunits reflects a high probability of AD risk. Regarding the above discovery, the following hypothesis is proposed: The aggregation of pathogenic proteins intensifies with AD progression, then proteasome becomes more active and facilitates the UPS selectively targets the degradation of abnormal proteins to maintain CNS proteostasis. In this paper, bioinformatics and support vector machine learning methods are applied and combined with multivariate statistical analysis of microarray data. Additionally, the concept of entropy was used to detect the disorder of proteasome system, it was discovered that entropy is down-regulated continually with AD progression against system chaos caused by AD. Another conception of the matrix determinant was used to detect the global coordination of proteasome, it was discovered that the coordination is enhanced to maintain the efficiency of degradation. The features of entropy and determinant suggest that active proteasomes resist the attack caused by AD like defenders, on the one hand, to protect themselves (entropy reduces), and on the other hand, to fight the enemy (determinant reduces). It is noted that these are results from biocomputing and need to be supported by further biological experiments.