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Targeting Mitochondrial Dysfunction & Toxicity Conference - Day 1


2014 Archived Content

WEDNESDAY, MARCH 19 


Day 1 | Day 2 | Brochure 

7:45-9:00 am Short Course Registration*

Morning Short Course

9:00 – 12:00 pm Imaging Mitochondria: Seeing the Action Up Close and Live

Highly effective methods of imaging mitochondria and their processes have emerged recently. These new methods enhance in vivo examination of the cells and allow for much more detail of these organelles. This short course will explore some of the most innovative and effective methods for seeing into the “cell engines” and visualizing their operations for better understanding of them.

Instructors and Topics: 

Automated 3D-Electron Microscopy Presents New Opportunities for Mitochondrial Research and Drug Development 

Robin Avila, Ph.D., Scientist, Renovo Neural, Inc. 

Non-Invasive Imaging of Retinal Mitochondrial Dysfunction in Age-Related Macular Degeneration and Diabetes 

Victor Elner, M.D., Ph.D., Ravitz Foundation Professor of Ophthalmology and Visual Sciences Professor, Department of Pathology, University of Michigan Kellogg Eye Center 

* Separate registration required 

 

12:00-1:25 Main Conference Registration

1:30 Chairperson’s Welcoming Comments

Elizabeth J. Lamb, Senior Conference Director, Cambridge Healthtech Institute


NEW DATA WITH WIDE IMPLICATIONS 

1:40 Mitochondrial Allostatic Load and Therapeutic Windows

Martin Picard, Ph.D., D.Hom., CIHR Postdoctoral Fellow, Center for Mitochondrial and Epigenomic Medicine, Children’s Hospital of Philadelphia and University of Pennsylvania

With the aim of preventing dysfunction and offsetting toxicity without destroying basic adaptive mitochondrial functions, Mitochondrial Allostatic Load identifies stressors to which mitochondria exhibit particular sensitivity, defines key elements of mitochondrial dysfunction, and describes molecular mechanisms by which mitochondrial damage accumulate and disrupt normal cellular physiology. As an example, we report a non-linear pattern of communication between mitochondria and nucleus, whereby increasing levels of a pathogenic mitochondrial DNA mutation cause bi-phasic reprogramming of nuclear gene expression.

MUSCLE, NEURODEGENERATIVE AND PSYCHIATRIC 

2:10 The Role of Mitochondria in the Cytopathogenesis of Neurodegenerative Disorders

Viktor Kis, Ph.D. Researcher, Laboratory of Proteomics, Eötvös Loránd University

Combining freeze-substitution followed by LR White embedding and highly senstive immunocytochemical methods we developed a protocol which gives superior antigen preservation and pleasing ultrastucture. In our hands this new technique revealed novel perspects of the localisation of the disease associated form of alpha-synuclein in postmortem human brain samples from patients with Parkinson’s disease. Using electron microscopic enzyme cytochemistry we could demonstrate cell type (principal cells, interneurons and astrocytes) specific differences in mitochondrial activity in the hippocampus of APP/PS1 transgenic mouse models of Alzheimer’s disease.

2:40 Adult Neurogenesis Transiently Generates Oxidative Stress

Noah M. Walton, Ph.D., Astellas Research Institute of America LLC

We hypothesized that the energetic demands of highly proliferative progenitors generates localized oxidative stress that contributes to ROS-mediated damage within the neuropoietic microenvironment. To confirm these findings in vivo, we identified a set of oxidation-responsive genes, which respond to antioxidant administration and are significantly elevated in genetic- and exercise-induced models of hyperactive hippocampal neurogenesis. While no direct evidence exists coupling neurogenesis-associated stress to CNS disease, our data suggest that oxidative stress is produced as a result of routine adult neurogenesis.

3:10 Refreshment Break in the Exhibit Hall with Poster Viewing

3:45 Increased Cellular Mitochondrial Content and Decreased Complex IV Function in Peripheral Blood Cells from ALS Patients

Johannes Ehinger, MD, Mitochondrial Medicine, Lund University

Peripheral blood cells are a readily available source of human mitochondria. Using a polarographic approach, mitochondrial function can be assessed in near physiologic conditions (intact cells submerged in the patient’s own plasma) or in permeabilised cells, at a level of individual respiratory complexes. As a first report from a project probing mitochondrial function in neurodegenerative disease, we report findings on mitochondrial function using thrombocytes and mononuclear cells from an amyotrophic lateral sclerosis (ALS) patient cohort.

4:15 Link between Cancer and Alzheimer’s Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Over-Proliferation and Deletion

Gjumrakch Aliev, Ph.D., GALLY International Biomedical Research Consulting LLC

Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer’s disease (AD). We speculate that mitochondrial involvement may play a significant role in the etiopathogenesis of cancer. Recent advances in the cell-cycle reentry of the terminally differentiated neuronal cells indicate that NO-dependent mitochondrial abnormal activities and mitotic cell division are not the only important pathogenic factors in pathogenesis of cancer and AD, but open a new window for the development of novel treatment strategies for these devastating diseases.

4:45 - 5:45 Welcome Reception in the Exhibit Hall with Poster Viewing 

6:00 Close of Day 1

 

Present a Poster 

CHI encourages attendees to gain further exposure by presenting their work in the poster sessions.

  • Your poster will be exposed to our international delegation
  • Receive $50 off your registration
  • Your poster abstract will be published in our conference materials
  • Your research will be seen by leaders from top pharmaceutical, biotech, academic and government institutes

To secure a poster board and inclusion in the conference materials, your abstract must be submitted, approved and your registration paid in full by February 14, 2014.



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