Project description:To delineate the mechanism by which human mitochondrial transcriptional factor A (hTFAM) suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment. One-way ANOVA was performed with the transcript clusters altered in PS1P117L cells compared with wild-type cells. Comparative analyses of PS1P117L cells and wild-type cells showed that the expression of genes involved in cellular assembly and organization, cellular function and maintenance, and tissue development were significantly altered.

2016-12-01 | GSE80244 | GEO

Topological data analysis in air traffic management: The shape of big flight data sets.

Project description: Not available

| S-EPMC11867395 | biostudies-literature

Systems level insights into the impact of airborne exposure on SARS-CoV-2 pathogenesis and COVID-19 outcome - A multi-omics big data study.

Project description: Not available

| S-EPMC8358088 | biostudies-literature

Unraveling Presenilin 2 Functions in a Knockout Zebrafish Line to Shed Light into Alzheimer's Disease Pathogenesis.

Project description: Not available

| S-EPMC9913325 | biostudies-literature

Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer's disease -conformist, nonconformist, and realistic prospects for AD pathogenesis.

Project description: Not available