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Thursday, April 26, 2012
1.Looking at the mouse genome and the human genome, it is seen that man and mice share ninety-nine percent of their DNA. Particularly looking at the brain, it is believed that the brain of humans share many of the same functions of mice at some point because the older parts the brain that existed came is also present in the mouse. It is believe that more of the middle parts of the brain which is where AD has been said to begin are considered the oldest parts of the brain. So using a mouse we would have the older part of the brain to test, which again deals with the portion of the brain that AD is said to begin, we can see very similar pathways the disease will take. The paper referenced different experiments where degeneration of the brain was induced to create symptoms similar to AD.
2. According to the blast the mouse and the rat have very similar APP as that in humans.
· Mus musculus amyloid beta (A4) precursor protein-binding (House mouse)
· Rattus norvegicus amyloid beta (A4) precursor protein-binding (Norway rat)
· Homo sapiens amyloid beta (A4) precursor protein-binding (Human)
· Macaca mulatta amyloid beta (A4) precursor protein-binding, (Rhesus monkey)
· Callithrix jacchus amyloid beta (A4) precursor protein-binding, (White-tufted ear marmoset)
3. I don’t think Alzheimer’s is subject to natural selection because although for many cases there is a specific genotype that may lead to AD and in others there isn’t this genotype, in most cases the actions of the disease doesn’t come into play until a person is older, past the reproductive stage. We don’t know when symptoms will come about or if they will at all in that state, but some people may not even live long enough so AD doesn’t affect them, directly.
4. If the APP is thought to be on chromosome 21 and individuals with trisomy 21 have and extra chromosome 21, they are likely to produce more APP. If an over production of APP lead to AD then they are likely to reach a state of AD at a faster rate and have it occur earlier in their life since that gene on chromosome 21 is creating that much more APP.
Bonus. It did talk about amyloid beta and tau involvement in AD. The paper went more in depth, Dr. Sturgill wasn’t as familiar with the actual role of tau in the brain, but he knew it lead to AD when tangles were formed. As far as the amyloid-beta both the paper and Dr. Sturgill talked about it forming the plaque and where it started, the fact that it spread throughout the brain and the apolipoprotein E had some involvement in the progression to AD.
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