Eugenia V. Trushina

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

The paper identifies preserved mitochondrial bioenergetics in asymptomatic Alzheimer's disease brains and suggests NAD+ precursor interventions could maintain cognitive function despite pathology.

The paper tests a small-molecule inhibitor of mitochondrial complex I in a schizophrenia mouse model, finding it improves mitochondrial function and behavioral deficits.

This paper describes the discovery and validation of C273, a mitochondrial complex I modulator that reduces Alzheimer's disease pathology by enhancing cellular resilience through AMPK-mediated pathways.

This study profiles mitochondrial respiration in IBM muscle tissue, identifying sex-specific impairments in respiration and OXPHOS complexes, along with correlations with disease severity.

The paper assesses a novel mitochondrial complex I inhibitor, C458, in vitro and in vivo, showing it protects against Aβ toxicity, improves brain energetics, and reduces inflammation in Alzheimer's disease models.

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.

This study identifies sex-specific metabolic alterations in IBM muscle tissue, showing changes in central carbon metabolism and correlations with clinical parameters.

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 study shows that inhibiting mitochondrial complex I with CP2 reduces pTau levels and improves cognitive and metabolic function in 3xTg-AD mice.

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