Chemweb Events

Targeting Mitochondrial Dysfunction and Toxicity Mar 19-20 2014
Conference: United States [in English]

Mitochondrial dysfunction has been identified as an important factor in diseases ranging from neurodegenerative conditions (ALS, Alzheimer's, Parkinson's Disease), epilepsy, psychiatric illness and autism, to cardiovascular disease, liver/kidney disease, diabetes and cancer. The wide-ranging impact of mitochondria in so many diseases makes them prime targets for therapeutics.
Additionally, medications for many diseases cause unwanted toxicity to the mitochondria. Mitochondrial toxicity is one of the leading causes of attrition in the drug development process, as well as in post-market drug withdrawals. Targeting Mitochondrial Dysfunction & Toxicity (the first conference of its kind in the US) will present the latest research in new targeting pathways, novel therapeutics, and methods to decrease or eliminate mitochondrial toxicity when developing therapeutics for many indications.

keywords:   mitochondria
Event Location:
60 School Street
Boston, Massachusetts 02108
United States

Organizer:
Kris Waterman (send an email)
250 1st Avenue
Needham, Massachusetts 02494
United States
Deadlines
Early registration: Friday, February 14, 2014
Posters: Friday, February 14, 2014
Session titles:

Session titles include:
-Mitochondrial Allostatic Load and Therapeutic Windows
-Mitochondrial Movement and Mood Stabilizer Treatment
-Postnatal Neurogenesis Generates Oxidative Stress
-Isolated Normal Mitochondrial Organelle Transplantation to Cancer Cells
-Targeting Mitochondria Function for the Treatment of Breast Cancer
-Mitochondria Are at the Center of Islet Beta-Cell Signaling and Metabolism-Secretion Coupling
-Identification of a Mitochondrial Target of Thiazolidinedione Insulin Sensitizers (mTOT): Relationship to Newly Identified Mitochondrial Pyruvate Carrier Proteins
-In Vitro Approaches to Assess Mitochondrial Toxicity and Mitochondria-Mediated Drug Toxicity: A Decade of Learning
-Novel Tools to Assess Mitochondrial Toxicity under Physiological Conditions