• Mitochondrial Function as a Therapeutic Target for Alzheimer's Disease

    Mitochondrial Function as a Therapeutic Target for Alzheimer's Disease

    Organizers: Howard Fillit (Alzheimer's Drug Discovery Foundation) and Sonya Dougal (The New York Academy of Sciences)Presented by the Alzheimer's Drug Discovery Foundation, the Brain Dysfunction Discussion Group, and The New York Academy of Sciences.
    Reported by Catherine Zandonella | Posted July 6, 2010


    Alzheimer's disease will strike one of every three adults. Although much is known about the telltale signatures of the disease—protein plaques and tangled nerve cell fibers in the brain—the true cause of this disease remains unknown.

    A number of lines of research point toward mitochondria, the cellular energy-producing organelles, as playing a causative role in Alzheimer's disease (AD). Numerous studies have found that people with AD experience declines in brain energy metabolism that begin years before the onset of symptoms. An individual's type of mitochondrial DNA, or haplotype, influences one's risk of Alzheimer's disease and other neurodegenerative disorders. Researchers came together at the New York Academy of Sciences on May 13, 2010, to discuss their latest discoveries and explore ways to harness therapeutics to repair mitochondria and treat AD.

    Use the tabs above to find a meeting report and multimedia from this event.

    Presentations are available from:

    Douglas C. Wallace (University of California, Irvine)
    Xiongwei Zhu (Case Western Reserve University)
    Tomas A. Prolla (University of Wisconsin – Madison)
    P. Hemachandra Reddy (Oregon Health & Science University)
    M. Flint Beal (Weill Medical College of Cornell University)
    William Kirby Gottschalk (Duke University)
    Stuart A. Lipton (Sanford | Burnham Institute for Medical Research)
    Shi Du Yan (Taub Institute of Columbia University)
    Jerry R. Colca (Metabolic Solutions Development Company)


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