The laboratory of Eugenia Trushina, Ph.D., is focused on mitochondrial dysfunction caused by environmental toxins, chemotherapy drugs, and genetic factors in multiple neurodegenerative disorders, including Huntington's disease and Alzheimer's disease, aging, and chemotherapy-induced peripheral neuropathy.

Her research interests involve the identification of the molecular mechanisms involved in the inhibition of mitochondrial dynamics and function in neurons. Her current projects involve the development of a panel of the specific biomarkers associated with early mechanisms of mitochondrial dysfunction involved in neurodegeneration that could be useful for early diagnosis and monitoring/predicting the progression of multiple diseases, including Alzheimer's disease. She is also testing novel mitochondria-targeted therapeutic approaches that could potentially reverse neurodegeneration and aging.

Dr. Trushina's research has been funded by the Mayo Clinic Alzheimer's Disease Research Center, the American Health Assistance Foundation, the Alzheimer Drug Discovery Foundation, and the National Institutes of Health.

Focus areas

• How do mitochondria become bad and contribute to disease progression? Dysfunction of mitochondria, the power plant of the cell, has been implicated in the etiology of multiple disorders, including neurodegenerative diseases, neuropathies and aging. Most importantly, mitochondrial dysfunction typically happens very early in disease progression. Dr. Trushina is focusing on better understanding the molecular mechanisms of early mitochondrial dysfunction. She is studying changes in mitochondrial motility, fission, fusion, ultrastructure and function in relationship to the impact of environmental toxins, chemotherapy drugs and genetic factors associated with different disorders.
• How can we identify mitochondrial dysfunction early? Mitochondrial dysfunction occurs early in progression of multiple disorders. Dr. Trushina's group is working on developing specific biomarkers that could help to identify changes in mitochondrial function in plasma, cerebrospinal fluid and peripheral tissue to predict the onset and progression of disease.
• What can we do to restore mitochondrial function? Dr. Trushina has identified novel molecules that restore mitochondrial dynamics in neurons. She and colleagues have demonstrated that in multiple model systems of Alzheimer's disease, restoration of mitochondrial dynamics and function significantly delays the onset and slows down the progression of disease. These data validate mitochondria as an important therapeutic target. Dr. Trushina's group is exploring whether such treatment could be applicable to other neurodegenerative diseases and aging.

Significance to patient care

Dr. Trushina's research will help to develop novel methods for diagnosis and treatment of neurodegenerative diseases to delay the onset of symptoms and improve quality of life for patients with Alzheimer's disease, Huntington's disease, Parkinson's disease and other neurodegenerative disorders.