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Mitochondrial Function in Aging and Disease
APS Cell and Molecular Physiology Section
Kevin E. Conley
G.A. Cortopassi, M. Harper, C. Leeuwenburgh, G. I. Shulman and D.J. Marcinek
The decline in mitochondrial function is a key part of aging and a number
of diseases. This functional loss means a reduced capacity for oxidative
ATP synthesis and increase susceptibility to apoptosis and cell death. This
symposium asks what is the basis of the loss of function and what aspects of
aging and disease cause a functional decline. The goal is to identify the
role of genetics, disease damage and secondary disease effects on the loss
of mitochondrial function. First, we ask what role damage to the
mitochondrial genome plays in mitochondrial neurodegenerative diseases
(e.g., Friedriech's ataxia) that develop with age (Cortopassi). The loss of
motor control due to mitochondrial defects in nerves will serve as an
example of the role of gene mutations and damage in the functional decline.
Second, the mitochondrial damage resulting from aging vs. oxidative stress
will be presented. The goal of the second two talks is to separate the
normal decline with aging (Harper) from the pathological damage that occurs
with oxidative stress and other noxious factors (Leeuwenburgh). In
specific, the role of oxidative damage in apoptosis will be presented.
Third, many diseases have secondary effects on mitochondria that reduce
function. These secondary effects will be explored by focusing on the role
of mitochondrial function in insulin resistance in diabetes (Shulman).
Finally, new, non-invasive approaches for measuring mitochondrial function
in vivo will be presented as an important future direction for investigating
the time course and extent of mitochondrial changes with aging and disease.
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