Grid statistics

rosetta@home
Work done: 6533.26
Average: 45.79
Resource share 100(100%)

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.

Journal Article Relating to Alzheimer's

Transgenic Models of Alzheimer’s Disease: Learning from Animals

Wendell's Response to Interveiw

I was pleasantly surprised by what we learned. Dr. Sturgil doesn’t do direct work with Alzheimer’s, but he was able to give a different perspective of it and shed light on things that we hadn’t found or heard about as in debt. I knew that Alzheimer’s is hereditary, but I didn’t link that to being on a chromosome, which makes it a little scarier since I have Alzheimer’s and dementia in my family. We learned that the earliest sign of Alzheimer’s was in someone who was twenty-nine, which was disturbing to all of us. From pictures it appeared as if the entire brain was under attack and that every part suffered from degeneration. We learned that there different types of cells of the brain and that the occipital lobe of the brain isn’t affected; which lead us to question why not Initially it was shocking to find that fetal cells used to combat the tau proteins were no match, however, I just read a paper that seemed to suggest that mutating tau would probably be a better solution,… though the side effects could be worse. The heritability, the fact that it is on chromosome 17, and the fact that everyone doesn’t have it, shows that it doesn’t deal with fitness because the symptoms occur after reproductive age. It must have been a mutation that occurred that has been passed down.

<http://www.pnas.org/content/96/10/5598.full.pdf>

Mara’s Interview Response

1. Describe your feelings about or response to the interview.
I feel like the interview went fairly well. I was really interested in what Dr. Sturgill knew about Alzheimer's. I was really surprised to learn that eye sight is unaffected by Alzheimer's.

2. What changes occurred for you as a result of your interview?
I had a better understanding and different perspective of the topic.

3. Did anything about it disturb you?
I didn't find anything disturbing.

4. Describe the connections you found between the interview and your research/classwork.
Individuals who develop early on-set Alzheimer’s have an inherited predisposition to develop the disease; it is the result of a heritable mutation. Dr. Sturgill believes that other animals are probably susceptible to neurodegenerative diseases.

Secondary Interview

This interview was with Sue Derdeyn, a family friend of Caroline's, on Thursday, February 16, 2012. Sue has unfortunately has had first hand experience in observing and dealing with Alzheimer's disease. She was kind enough to share her personal experiences with us!  

What’s your experience with individual who have Alzheimer’s?

My mom developed Alzheimer's when she was in her early 50's and lived with it for about 15 years. I was in college when her first symptons appeared. We moved to Florida for a new job for my dad and my mom had a very hard time remembering the new streets and neighborhoods and was constantly repeating stories and forgetting people's names. At the time, there was no test for diagnosing Alzheimer's so we took her to Nuerologists and Psychiatrists for evaluations and they basically ruled out everything else it might be to come up with the diagnosis. I recalled one evaulator asked my mom if she could remember the names of the streets we had taken to get tot he doctors office and she could not. Her short term memory went first and then her long term memory was affected as well. This was in the mid-1980's and there was no medicine or treatment for the disease. My dad was able to keep my mom at home. She soon needed a daytime caregiver to be with her to keep her safe. Cooking was dangerous as she would forget to turn off the stove. She got lost once when she went on a walk in the neighborhood. My dad took care of her each night he was home from work. Mom never got violent and maintained a pleasant, polite demeanor- just as she had been before she got sick. Eventually, she had trouble eating and got pnemonia from aspirating her food which is what led to her death.

Are you familiar with any organizations or foundations dedicated to raising funds/promoting awareness of the disease?

The Alzheimer's Association is a great organization dedicated to raising funds for research, raising awareness in the community of the disease, providing famlies with respite assisitance (basically giving the caregiver some time off) and offering support groups for the caregivers, as well as for the patient. There are branches in most major cities, including a very active one in St. Louis that I got involved with as a volunteer and part-time accountant back in the early 1990's. 

Are you familiar with any of the current research being done to find a cure for Alzheimer's?

I am not current on the latest research...hopefully they are getting close! 

We would like to thank Sue again for her time and sharing her personal story with us! We really appreciate it! 

Interview

Dr. Sturgill graduated from Omaha with an undergraduate and masters degree in experimental psychology. He then obtained his doctorate in cognitive psychology in California. Dr. Sturgill has been teaching at Rockhurst University for about 24 years. He currently teaches cognitive neuroscience, cognition, sensation and perception, psych of language, history of psych, stats, experimental methods, and a course at KCUMB. Dr. Sturgill has done no previous research with Alzheimer’s or other types of dementia. When research of the brain occurs, there are three classes of subjects: lesion patients, paralogically intact, and animal models. Lesion patients are individuals who already have damage to the brain. The paralogically intact is the group of individuals with healthy, normal brains. Animal models, such as primates or rats, are used as a third group. Alzheimer’s begins in the temporal lobe, causing problems forming new memories. Individuals with Alzheimer’s typically are fine as long as they’re in familiar surrounds because they can rely on older memories. However, problems arise when they go on vacation or visit new places. Alzheimer’s then progresses along the temporal lobe and then into the the parietal lobe, causing some spacial and motor problems. From the parietal lobe, it progresses into the frontal lobe. However, the occipital lobe seems to be unaffected. The main differences between the early stages of Alzheimer’s disease and aging is the speed of progression and occurrence of cell death. In normal aging, Dr. Sturgill said the “processing speed of an old brain slows down, but there’s not a loss of intelligence or cognitive abilities.... The extent of cell degeneration in Alzheimer’s doesn’t occur within old ages. A scan of an old brain that is 70 or 80 years old will look healthy.”  The progression of alzheimer’s is much faster than normal aging and usually occurs at a younger age than age related memory losses. The early-set Alzheimer’s occurs in the late 40’s or early 50’s, which Dr. Sturgill said is “way too early for normal age related kinds of losses.” The second kind of Alzheimer’s, late on-set, tends to present after age 65 “which is approximately the same time age related memory loss begins,” according to Dr. Sturgill. In a brain with Alzheimer’s there is lots of cell death and the guri are thin. Tau and amaloid proteins, which are related to Alzheimer’s disease, are present in all individuals. Some build up of protein occurs in old age, but not to the extent of those individuals with Alzheimer’s.

When explaining the structure of the brain and it’s relation to Alzheimer’s Dr. Sturgill says, “You know there are … difference in the microstructure, for instance, between the left hemisphere and the right hemisphere in certain areas just the cell sizes are different, their dendritic  arbors are different… so there could be something about those particular kinds of cells that are in the entorhinal cortex and those cells that are in the hippocampus, which are different kinds of cells… that are particularly… producing these filament problems in the cells in generating tau.” From here we went on to a discussion about how tau works, it has been recently been found that tau spreads from cell to cell, which Dr. Sturgill compare to an infection. Dr. Sturgill insisted that there had to be some role for tau and that the difference between individuals with Alzheimer’s and people without Alzheimer’s was that those with Alzheimer’s patients had large amounts of the tau protein. In understanding the new evidence and knowing the pathways of the spread Dr. Sturgill says, “they’ve known for a while that Alzheimer’s along that kind of pathway from the entorhinal, to the hippocampus, to the medial temporal area and that’s just where these neurons are connected one to the next. So finding that they know how it spreads now may actually help generate some sort of a treatment to stop it, if they can stop the spread of tau then they can stop  Alzheimer’s.” In understanding this and earlier highlighting that the occipital lobe doesn’t seem to be affected by the disease, it easy to question why this is. Dr. Sturgill clears this up by explaining that though there are pathways that do go from the occipital lobe to the temporal lobe, but there are different types of cell structures that are in the occipital cortex so proteins produced may play a role in why tau doesn’t seem to affect this area of the brain.

When talking about grid computing, which he knew as parallel processing, he agreed that is certainly possible for a cure to come about as a result of a grid.

In talking about evolution and its relation to Alzheimer’s Dr. Sturgill says, “It [Alzheimer’s] is some kind of a mutation and if one of those mutations turned out to have some kind of benefit  in the long run, overtime it showed up then that might be a evolutionary kind of change.” It seems as though animals should be just as susceptible to have a neurodegenerative disease, like that of Alzheimer’s, but we were all unsure if that is the case.

When looking at a few possible solutions he states that the precursors of the production of the beta-amyloid, which creates plaque in the brain, could be found that could lead to stopping the production or overproduction of the beat-amyloid. It had been found that a vaccine was something in the works for stopping or slowing down Alzheimer’s. According to Dr. Sturgill “… the treatments have been aimed primarily at neurotransmitters particularly at acetylcholine because it affects the acetyl cholinergic system. This entorhinal cortex is very near the basil forebrain, where the temporal lobe and the frontal cortex all come together. The very center base of the fore brain and that’s where these neurons are the generate acetylcholine in the basal forebrain. So right away you have this cholinergic problem and they spread out throughout the cortex, that cholinergic system and so then there is this loss of that acetylcholine. So trying to up that has been one effort and what it’s done  primarily is slow down or sort of retard the time it takes for people to be admitted to a home where they have to spend the rest of their time. That in itself, that slowdown, saves billions of dollars in medical costs, but that’s been primarily the effort to aim at neurotransmitters at this point.”

Dr. Strugill had read earlier in experiment dealing with Parkinson’s disease how fetal cells were used to combat tau proteins, but it was found that the tau proteins even overtook the fetal proteins, which was unexpected.

We would like that to thank Dr. Sturgill for taking his time to do this interview and for furthering our knowledge of Alzheimer’s and how the brain works.

 

 

http://brainmind.com/BrainLecture1.html