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Ackerman says that knowledge of how modifier genes work to prevent such damage
may present new therapeutic options for treating diseases caused by protein
misfolding. For example, a modifier gene that creates a pathway to prevent
cumulative damage in the cell could be chemically activated to speed up the
mechanism for damage control.
"By working on these compensatory aspects of a disease, even though you haven't
fixed the primary cause, you may be able to stop or slow its progression," she
says," and that could be enormously helpful." 
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Ackerman is also using modifier genes to suppress oxidative stress in the brain,
which has been linked to diseases such as Alzheimer's, Parkinson's, and
amyotrophic lateral sclerosis, or "Lou Gehrig's disease." Oxidative stress
occurs when chemicals called free radicals accumulate in a cell and damage
proteins, DNA, and other cellular components. Recently, Ackerman's lab
identified a gene that, when mutated in mice, results in high levels of
oxidative stress throughout the brain. Mice with this genetic mutation develop
motor problems associated with neuron loss soon after birth and die around six
weeks of age.
She has also identified a modifier gene that, when placed in the mutant mice,
reduces the neuronal damage caused by oxidative stress. Through a breeding
process called backcrossing, Ackerman transferred the modifier gene into a group
of mutant mice. Preliminary studies show that those with the modifier gene are
able to sidestep the most severe aspects of the disorder and live
longer—more than two years. In addition, the mice develop the first
symptoms of disease much later in life.
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