Eugenia Trushina

TL;DR: The role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease are discussed.

TL;DR: Direct and functional evidence is provided that htt is involved in fast axonal trafficking in mammals and mhtt-mediated aggregation sequesters htt and components of trafficking machinery leading to loss of mitochondrial motility and eventual mitochondrial dysfunction.

TL;DR: This review discusses similarities among HD, Friedreich ataxia and xeroderma pigmentosum, which provide insight into shared mechanisms of neuronal death, and focuses on Huntington's disease.

TL;DR: The approaches described include restoring oxidative phosphorylation and glycolysis, increasing insulin sensitivity, correcting mitochondrial dysfunction, ketone-based interventions, acting via hormones that modulate cerebral energetics, RNA therapeutics and complementary multimodal lifestyle changes.

TL;DR: Global metabolic changes in plasma and cerebrospinal fluid from the same individuals with different AD severity are determined and metabolomics could advance the understanding of the early disease mechanisms shared in progression from CN to MCI and to AD.