Progress in mitochondrial and omics studies in Alzheimer's disease research: from molecular mechanisms to therapeutic interventions.

Alzheimer's disease (Alzheimer's disease, AD) is a progressive neurological disorder characterized by memory loss and cognitive impairment. It is characterized by the formation of tau protein neurofibrillary tangles and ß-amyloid plaques. Recent studies have found that mitochondria in neuronal cells of AD patients exhibit various dysfunctions, including reduced numbers, ultrastructural changes, reduced enzyme activity, and abnormal kinetics. These abnormal mitochondria not only lead to the loss of normal neuronal cell function, but are also a major driver of AD progression. In this review, we will focus on the advances of mitochondria and their multi-omics in AD research, with particular emphasis on how mitochondrial dysfunction in AD drives disease progression. At the same time, we will focus on summarizing how mitochondrial genomics technologies have revealed specific details of these dysfunctions and how therapeutic strategies targeting mitochondria may provide new directions for future AD treatments. By delving into the key mechanisms of mitochondria in AD related to energy metabolism, altered kinetics, regulation of cell death, and dysregulation of calcium-ion homeostasis, and how mitochondrial multi-omics technologies can be utilized to provide us with a better understanding of these processes. In the future, mitochondria-centered therapeutic strategies will be a key idea in the treatment of AD.

Microarray Data Analysis of Molecular Mechanism Associated with Stroke Progression.

This study aimed to explore the molecular mechanism of stroke and provide a new target in the clinical management. The miRNA dataset GSE97532 (3 blood samples from middle cerebral artery occlusion (MCAO) and 3 from sham operation) and mRNA dataset GSE97533 (3 blood samples from MCAO and 3 from sham operation) were obtained from GEO database. Differentially expressed mRNA (DEGs) and miRNAs (DEMIRs) were screened out between MCAO and sham operation groups. Then, DEMIR-DEG interactions were explored and visualized using Cytoscape software. Moreover, the enrichment analysis was performed on these DEMIRs and DEGs. Furthermore, protein-protein interaction (PPI) network was constructed. Finally, the DEG-target transcription factors (TFs) were investigated using the WebGestal software. The current bioinformatics analysis revealed 38 DEMIRs and 546 DEGs between MCAO and sham operation groups. The DEMIR-DEG analysis revealed 370 relations, such as miR-107-5p-Furin. The top 10 up- and downregulated DEMIRs were mainly enriched in pathways like cAMP signaling pathway. The PPI network analysis revealed 2 modules. The target DEGs of the 10 up- and downregulated DEMIRs in 2 modules were mainly assembled in functions like ATP binding and pathway including ABC transporters. Furthermore, the DEG-TF network analysis identified 5 outstanding TFs including androgen receptor (AR). miR107-5p might take part in the progression of stroke via inhibiting the expression of Furin. TFs like AR might be used as a novel gene therapy target for stroke. Furthermore, cAMP signaling pathway and ATP binding function might be a novel breakthrough for stroke treatment.