Behavior Presentation Evaluation

Genetics, Brain Structure, and Behavior Presentation Evaluation
Ryan Banta
Psy/340
June 13, 2011
Kristin Merritte

Genetics, Brain Structure, and Behavior Presentation Evaluation
In the third week of Biological psychology, or at is otherwise known, Psy340, each team in the class was assigned to do a presentation of an illness. While the team I was on concentrated on Bipolar disorder, the other teams chose to do something else entirely, which was just fine since it would be pointless doing an evaluation. After looking at the presentation that the other teams had done, I had decided on Team C’s Presentation of Huntington’s Disease. The main reason I chose to do the presentation on Huntington’s disease that I know next to nothing on Huntington’s
and it would be a great learning experience for me.
Huntington’s Disease is defined as a hereditary disorder with mental and physical deterioration leading to death.
Although characterized as an “adult on-set” disease, it can affect children as well (Medterms, 1998). Huntington’s is a genetic disorder that main affects people in their 40’s and 50’s (Team C, 2011). I mainly affects the brain which leads to a gradual loss of control of movement along with memory loss and a loss of mental ability (Team C, 2011). I suppose you could say it is essentially a breakdown of the brain and the functions that are accompanied with it (Team C, 2011). With Huntington’s disease comes certain personality changes and depression along with some other mental illnesses (Team C, 2011). As of now there is no known cure but there have been a few case studies researching the possibility of a cure (Team C, 2011). Huntington’s disease has a pattern known as “autosomal dominance” (Team C, 2011). Autosomes Are the chromosomes inside the cells of the body aside from the sex chromosomes (Team C, 2011). This is where our body’s genetic information is stored and located (Team C, 2011). The genetic abnormality that is normally associated with Huntington’s disease is located on the fourth chromosome and the three bases arranged along the chromosome happen in a repeated sequence (Team C, 2011). An excess amount of the repeats leads to Huntington’s disease (Team C, 2011). Any more than 35 reps of this particular sequence is often attributed to Huntington’s but
people that have up to 39 repeats may not have Huntington’s disease (Team C, 2011).
There are several ways that Huntington’s disease causes not only damage but change to the brain (Team C, 2011). Clusters of Huntington’s disease provide steady stress to the healthy cells until they ultimately fail (Team C, 2011). It also affects the brain and the spinal cord (Team C, 2011). The failing cells is what basically causes the symptoms of Huntington’s disease (Team C, 2011).
As it has been mentioned previously, there are certain functional changes that comes with Huntington’s disease, but there are also some behavioral changes as well (Team C, 2011).
It is known that changes happen to the personality or even the mood with Huntington’s disease (Team C, 2011). This is actually the earliest detectable signs of this disease (Team C, 2011). Issues with memory and unusual uncontrollable movements that occur usually come later (Team C, 2011). The personality changes can occur as early as 10 years before the actual abnormal movements are even noticed but the symptoms will become progressively worse at that point (Team C, 2011). On average, Death due to Huntington’s disease occurs anywhere from 15 to 20 years after the first symptoms surface (Team C, 2011). This is a result of health decline and a cause of death could be choking on food due to difficulty swallowing (Team C, 2011). The main area of the brain that is affected by Huntington’s disease is in the Basal Ganglia (Team C, 2011). More specifically the Neostriatum which is comprised of the nucleus and the Putamen (Team C, 2011). The Basal Ganglia is located within the cerebral hemispheres in the telecephalon region of the brain (Team C, 2011).
As it has been said previously, Huntington’s disease is hereditary (Team C, 2011). That being said, if you inherit a copy of the gene for the disease from either parent, you will develop it at some point in your life (Team C, 2011). If you have one parent that
has it, you have a 50 percent chance of inheriting it (Team C, 2011).
When it comes to Huntington’s disease, there is no cure at this point in time (Team C, 2011). There is no treatment that can alter the course of Huntington’s disease but there are medications that can lessen the symptoms of movement and psychiatric disorders (Team C, 2011). These medications help patients cope with the symptoms that are attributed to Huntington’s disease (Team C, 2011). Medications such as Valium and Klonopin help with the jerking and writhing movements along with the muscle rigidity that is caused by the breakdown of the brain that Huntington’s causes (Team C, 2011). There are also therapies available to help Huntington’s disease patients understand and learn to live with the numerous factors associated with the disease such as behavior, motor regression and speech delays (Team C, 2011).
When it comes to Huntington’s disease, genetics plays a very large role (Team C, 2011). If a parent has Huntington’s disease, The chances are very large that their children will get this disastrous disease as well (Team C, 2011). The exact chances are 50 percent with one parent and 100 percent with 2 (Team C, 2011). There is a possibility of the gene being dormant and never becoming active but the chances of those are next to none sadly (Team C, 2011).
At first glance of this presentation, I would have to admit I thought there would be more color to it. The first slide shows a nervous system profile in the top left hand corner and an orange strip where the title of the presentation is. The main problem I had with the visual aspects of the presentation was the fact that the team did not stick with one font throughout the whole presentation. On the first slide along there was a total of three different fonts which included Times New Roman, Calibri and Perpetua. Aside from those flaws, I believe that the presentation as a whole followed a very basic style. It all flowed nicely and kept to the same layout on every slide.
When it comes to the organization of the presentation, I would have to say except for a few small errors, I liked the way the presentation was laid out. When it comes to the content of the presentation it flowed very nicely except for a few spots. In slide number ten, the title was labeled “The role of genetics on the onset of the illness” yet it didn’t really talk about the actual genetics of the disease, but spoke about getting tested for it. The subject about genetics was actually discussed with the description of the actual illness itself. Aside from that little slip up I honestly have no complaints about the presentation. All in all, this presentation was very well laid out and gave the right information.

Reference
Medterms. (March, 1998). Huntington Disease Definition. Retrieved from http://www.medterms.com/script/main/art.asp?articlekey=3820
Team C. (June, 2011). Genetics, Brain structure, and behavior presentation. Retrieved from University of Phoenix Team C forum.