with huntingtons the cag codon on the anti-apoptosis gene huntingtin repeats causes cumulative gunk at particular kinds of neurons; the disease depends on having large numbers of CAG repeats
It reminds me very much of AGE proteins as well as the opportunity to develop gene regulation drugs that modify cytoprogramming
I think people here that would like to develop new longevity treatments would value reading the literature on huntingtons treatments
http://en.wikipedia....wiki/Huntingtin
Huntington's disease is caused by a mutation in the Huntingtin gene, where the CAG repeats more than 35 times and is unstable. These expanded repeats lead to production of a huntingtin protein that contains an abnormal number of glutamines at the N-terminal. This makes it part of a class of neurodegenerative disorders known as trinucleotide repeat disorders or polyglutamine disorders.
Enzymes in the cell often cut this elongated protein into fragments. The protein fragments form abnormal clumps inside nerve cells and may attract other, normal proteins into the clumps. These nerve cells do not function properly and ultimately die. This process is particularly likely to occur in the striatum (a part of the brain that coordinates movement) primarily, and the frontal cortex (a part of the brain that controls thinking and emotions).
People with 36 to 40 CAG repeats may or may not develop the signs and symptoms of Huntington disease, while people with more than 40 repeats will develop the disorder during a normal lifetime. When there are more than 100 CAG repeats, the person develops a severe form of HD known as Juvenile HD. Therefore, the number of CAG (the sequence coding for the amino acid glutamine) repeats influences the age of onset of the disease. No case of HD has been diagnosed with a count less than 36.[1]
Edited by treonsverdery, 29 July 2008 - 10:11 PM.
