Dervis A. M. Salih

The paper uses polygenic risk scores to analyze genetic contributions to neurodegenerative diseases across brain cell types, finding shared and disease-specific genetic risks.

drugMR uses multi-omics data to identify potential drug targets and adverse effects by integrating GWAS and pQTL statistics with various statistical methods.

The paper identifies an oligodendrocyte DNA methylation signature in Alzheimer's disease that is preserved across brain regions and disease stages, and is associated with altered gene expression in OLGs.

The paper identifies genetic factors associated with Alzheimer's disease progression using GWAS and longitudinal data, finding distinct genetic drivers from disease risk.

The paper identifies gene expression changes in microglia around Aβ plaques in human Alzheimer's disease tissue and finds cross-species concordance with mouse data.

This study shows that PSEN1 mutations disrupt regulated intramembrane proteolysis in astrocytes, leading to enhanced inflammatory responses and contributing to familial Alzheimer's disease progression.

This study shows microglia produce ABri peptide in FBD, contributing to amyloid plaques and neurodegeneration, and suggests ITM2B/BRI2 is involved in microglial disease responses.

This paper introduces a new mouse model, NLFTaum/h, that shows ageing and amyloid-β can initiate tau pathology without MAPT mutations, revealing interactions between age, Aβ, and human tau.

The paper uses long-read RNA-seq to study splicing changes in an Alzheimer's mouse model, identifying novel transcript isoforms and alternative splicing events in response to amyloid-beta.

The paper identifies a genetic variant in OAS1 linked to increased Alzheimer's disease risk and severe COVID-19 outcomes, showing its role in microglial inflammation.

This study investigates how TREM2 influences microglial anti-inflammatory responses and shows that reduced TREM2 expression impairs anti-inflammatory gene expression and STAT6 levels.

This study examines how rising amyloidβ levels affect synaptic transmission, microglial response, and cognition in APPSwe/PSEN1M146V transgenic mice before and after plaque formation.

The paper identifies 5 new Alzheimer's risk loci by comparing mouse amyloid microglial response with human GWAS gene-based SNPs.

This paper compares the effects of amyloid-beta plaques and Tau tangles in mouse models of dementia, showing that tangles cause severe neurodegeneration while plaques affect synaptic transmission and immunity earlier.