Cory C. Funk

The paper shows that modulating mitochondrial complex I in advanced Alzheimer's disease improves metabolic resilience through coordinated mitochondrial and lipid metabolism.

This study shows that reducing mitochondrial complex I activity in mice induces AD-like transcriptomic changes, which are partially reversed by a complex I inhibitor.

The paper validates and expands a serum protein signature associated with APOE genotypes, identifying new protein associations and potential targets for Alzheimer's disease prevention.

The paper identifies APOE genotype-related metabolite associations with biological age and bioenergetics in humans, showing counterintuitive patterns in {varepsilon}2 and {varepsilon}4 carriers.

The paper identifies a conserved Aβ amyloid 'responsome' in human and mouse AD brains, showing how amyloid scaffolds proteins involved in disease pathology.

The paper provides a public resource of single nucleus RNA sequencing data and multiscale networks from Alzheimer's disease and non-disease individuals, linking genetic variants to molecular features and revealing novel disease biology.

The paper constructs a genome-scale transcriptional regulatory network of the human placenta using genomic and transcriptomic data, identifying key regulators of preterm birth.

The paper uses Fokker-Planck diffusion maps to analyze microglial transcriptomes, revealing substates associated with Alzheimer's pathology.

This study shows that deletion of Abi3/Gngt2 affects amyloid β and tau pathologies differently with age in AD models.

This study identifies blood-based biomarkers associated with Alzheimer's disease genetic risk variants in a large cohort of healthy adults, showing effects from early adulthood and sex-specific patterns.

The paper compares microglial transcriptomic responses to Aβ peptide aggregates ex vivo and in vivo, finding distinct responses and highlighting the limitations of using ex vivo models to predict in vivo behavior.

The paper shows that partial inhibition of mitochondrial complex I protects against neurodegeneration in Alzheimer's mice by improving energy homeostasis, synaptic function, and reducing inflammation.

This paper performs a large-scale eQTL meta-analysis across cerebral cortical and cerebellar brain regions, identifying distinct eQTL patterns and demonstrating improved power over existing studies.

The paper develops a workflow to identify transcription factor binding sites across 27 human tissues using DNase-seq data, resulting in a comprehensive footprint atlas with high-quality predictions.

iREAD detects intron retention events from RNA-seq data by analyzing read depth and distribution patterns, producing a list of retained introns for further analysis.

The paper identifies differences in bile acid pathways for cholesterol clearance in Alzheimer’s disease by analyzing transcriptomes and metabolomics data from brain samples.

The paper presents tools for ensuring FAIRness in big biomedical data analysis through a case study on creating a transcription factor binding site atlas from ENCODE data.

The paper constructs a brain-specific transcriptional regulatory network model to identify core transcription factors involved in psychiatric and neurodegenerative diseases.

Coexpression meta-analysis of 2114 human brain RNA-seq samples across the AMP-AD consortium identifies five consensus Alzheimer's disease transcriptional clusters, including two sex-heterogeneous clusters and a previously unreported proteostasis cluster.

This study shows that B6.HttQ111/+ mice exhibit early transcriptional and proteostatic deficits before synapse loss and neurodegeneration in HD.