Collaborating Investigators

Nathan Staff, M.D., Ph.D.

Nathan Staff, M.D., Ph.D.

Nathan P. Staff, M.D., Ph.D., studies disorders that damage the peripheral nervous system, including motor neurons, either through toxic mechanisms (chemotherapy), degeneration (amyotrophic lateral sclerosis) or inflammatory mechanisms. Dr. Staff uses both laboratory model systems and human clinical trials in his research. The long-term goal of Dr. Staff's research is to develop treatments in the laboratory setting and apply them in human clinical trials.

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Michael Ackerman, MD., Ph.D.

Dr. Ackerman

In the Mayo Clinic Windland Smith Rice Sudden Death Genomics Laboratory, Dr. Ackerman and his colleagues have research interests that include genomics, mutational analysis and novel gene discovery related to the cardiac channelopathies such as long QT syndrome, catecholaminergic polymorphic ventricular tachycardia and sudden unexplained death, including sudden infant death syndrome (SIDS), and inherited sarcomere diseases such as hypertrophic cardiomyopathy.

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Timothy Nelson, M.D., Ph.D.


The research of Timothy J. Nelson, M.D., Ph.D., focuses on cardiovascular regeneration using bioengineered stem cells. His work is directed at improving scientists' ability to discover, diagnose and ultimately treat mechanisms of degenerative diseases such as cardiomyopathy that weaken the heart muscle and lead to progressive heart failure.

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Alan D. Marmorstein, Ph.D.

Dr. Marmorstein

Research in the laboratory of Alan D. Marmorstein, Ph.D., is driven by the goal of restoring or preventing vision loss due to common and inherited eye diseases and trauma. Dr. Marmorstein studies how mutations in certain genes cause inherited forms of macular degeneration, how pressure is regulated within the eye and how some organisms regenerate their eyes in response to injury. The lab uses this information to identify and test new therapies, such as stem cells, for diseases like macular degeneration and glaucoma.

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Robert Huebert, M.D.


The research program of Robert C. Huebert, M.D., focuses broadly on liver regenerative medicine, with a focus on understanding and treating the cholangiopathies, a diverse group of diseases targeting the biliary tree. Dr. Huebert's laboratory seeks to understand the molecular mechanisms that drive biliary development, regeneration and repair, including the signaling pathways and epigenetic events that drive these processes.

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Dennis Wigle, M.D., Ph.D.


Research in Dr. Wigle's  laboratory is directed along two main project lines:

Thoracic Oncology: The application of gene expression biomarkers for the molecular staging of non-small cell lung cancer (NSCLC) is an emerging field with the promise of clinical translation.

Lung organogenesis: Understanding of the molecular mechanisms involved in growth and development of the normal lung are fundamental to harnessing these processes for clinical tissue regeneration. We use the mouse as a model for this work, and are interested in the potential utility of lung stem cells for regenerative strategies.

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Yogish Kudva, M.B.B.S


The research of Yogish C. Kudva, M.B.B.S., centers on improving existing treatments and developing novel therapies for patients with type 1 diabetes. In particular, Dr. Kudva is interested in developing an effective artificial pancreas system to improve outcomes for patients with type 1 diabetes. Additionally, his research contributes to the creation of new and better cell replacement therapies for patients with type 1 diabetes.

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Yasuhiro Ikeda, D.V.M., Ph.D.


The long-term goal of Yasuhiro Ikeda, D.V.M., Ph.D., is to develop efficient and safe gene and cell therapy platforms for diabetes and hypertensive heart disease.

Dr. Ikeda's main research interests include generation of embryonic stem cell-like stem cells from patients' skin and blood cells (induced pluripotent stem [iPS] cell technology), generation of insulin-producing cells from iPS cells as novel cell therapy for diabetes, development of pancreatic islet-targeted gene transfer vectors for diabetes gene therapy, and use of heart-targeted cardiac hormone gene therapy for hypertension and hypertensive heart disease.

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Leonard Petrucelli, Ph.D.


The laboratory of Leonard Petrucelli, Ph.D., is ushering in a new era of neurodegenerative disease research. Dr. Petrucelli's team has been at the forefront of research investigating the cellular mechanisms that cause neurodegeneration in diseases characterized by abnormal protein aggregation, such as Alzheimer's disease, frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). In expanding upon his commitment to understanding the causes of such diseases, Dr. Petrucelli is now emphasizing translational research geared toward identifying and developing therapies for treatment and prevention.

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Charles Howe, Ph.D.


The research of Charles L. Howe, Ph.D., is focused on discovering, characterizing, understanding and therapeutically manipulating the immunological responses to trauma, injury, loss of homeostasis, degeneration, autoimmunity and infection in the central nervous system with the goal of protecting neurons, axons and neural circuits.

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Guojun Bu, Ph.D.


Guojun Bu, Ph.D.'s laboratory investigates the roles of low-density lipoprotein receptor (LDLR) family and their ligands in the central nervous system and in the pathogenesis of Alzheimer's disease (AD).

LDLR family members, including LDL receptor-related protein 1 (LRP1) and LDLR, regulate the metabolism of amyloid-β (Aβ) peptide and apolipoprotein E (apoE). While Aβ is the primary toxic molecule in AD brains and a major component of amyloid plaques, an isoform of apoE (apoE4) is a strong risk factor for late-onset AD. Our laboratory is dissecting several major pathways in the brain that modulate the brain metabolism of Aβ and apoE, with specific focus on LRP1 and LDLR.

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Robert Diasio, M.D.


Robert B. Diasio, M.D., is the director of the Mayo Clinic Cancer Center. His research focuses on understanding how genetic factors can affect the efficacy of anti-cancer agents and can also be potential predictors of individuals at risk of severe, and potentially life-threatening, adverse drug toxicities.

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