Microsoft Word Kurzweil, Ray The Singularity Is Near doc

Mitochrondrial Mutations.
Another aging process is the accumulation of mutations in the thirteen genes in the 
mitochondria, the energy factories for the cell.
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These few genes are critical to the efficient functioning of our cells 
and undergo mutation at a higher rate than genes in the nucleus. Once we master somatic gene therapy, we could put 
multiple copies of these genes in the cell nucleus, thereby providing redundancy (backup) for such vital genetic 
information. The mechanism already exists in the cell to allow nucleus-encoded proteins to be imported into the 
mitochondria, so it is not necessary for these proteins to be produced in the mitochondria themselves. In fact, most of 
the proteins needed for mitochondrial function are already coded by the nuclear DNA. Researchers have already been 
successful in transferring mitochondrial genes into the nucleus in cell cultures. 
Intracellular Aggregates.
Toxins are produced both inside and outside cells. De Grey describes strategies using 
somatic gene therapy to introduce new genes that will break down what he calls "intracellular aggregates"—toxins 
within cells. Proteins have been identified that can destroy virtually any toxin, using bacteria that can digest and 
destroy dangerous materials ranging from TNT to dioxin. 
A key strategy being pursued by various groups for combating toxic materials outside the cell, including 
misformed proteins and amyloid plaque (seen in Alzheimer's disease and other degenerative conditions), is to create 
vaccines that act against their constituent molecules.
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Although this approach may result in the toxic material's being 
ingested by immune system cells, we can then use the strategies for combating intracellular aggregates described 
above to dispose of it. 
Extracellular Aggregates.
AGEs (advanced glycation end-products) result from undesirable cross-linking of useful 
molecules as a side effect of excess sugar. These cross-links interfere with the normal functioning of proteins and are 
key contributors to the aging process. An experimental drug called ALT-711 (phenacyldimenthylthiazolium chloride) 
can dissolve these cross-links without damaging the original tissue.
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Other molecules with this capability have also 
been identified.