Colette Blach

The paper analyzes metabolites in AD patients to show inflammation and sEH dysregulation, with sex and disease stage differences, and identifies markers of disease progression and cognitive resilience.

The paper uses whole-body metabolic models to link gut microbiota to metabolic changes in Alzheimer's disease, identifying key microbial drivers and metabolites involved.

This study links medication use to distinct gut microbial features in anxiety and depression, showing antidepressants have a larger effect on microbiota than diagnoses.

This study identifies widespread metabolic dysregulation in Alzheimer's disease brain tissue, linking it to tau pathology and highlighting potential pathomechanisms.

The paper links indoxyl sulfate, a gut microbiome-derived metabolite, to anxiety symptoms and specific brain connectivity patterns in patients with depression.

The paper uses targeted metabolomics to analyze changes in acylcarnitines, amines, and lipids in response to citalopram/escitalopram treatment in MDD patients, identifying metabolic correlates of treatment response.

The paper identifies serum metabolites associated with brain amyloid-beta deposition, cognitive dysfunction, and progression to Alzheimer's disease.

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 investigates sex and APOE ε4 genotype effects on metabolic alterations in Alzheimer’s disease using stratified analysis of serum metabolites.

This study identifies metabolites and pathways in serum and brain tissue associated with cognitive impairment and develops models to predict antecedent cognitive decline in older adults.

The paper identifies altered bile acid profiles in Alzheimer's disease, linking them to cognitive impairment and genetic variants through a large study.

The paper identifies associations between serum bile acid metabolites and AD biomarkers in the A/T/N framework, suggesting a potential role for bile acid pathways in AD pathophysiology.