Megan Zhou
No author given, but is based on materials provided by the University of Pennsylvania School of Medicine.
Published: May 13, 2014
http://www.sciencedaily.com/releases/2014/05/140513175211.htm
Summary:
A research team from 2008 had shown that mutations in two proteins associated with familial Alzheimer's Disease disrupted the flow of calcium ions in neurons; the same team, now led by Kevin Foskett, has found that suppressing the hyperactivity of calcium channels subdued the FAD-like symptoms in mice. Foskett says that these new observations suggest approaches for therapies based on modulating calcium signaling, as current treatments for the pathology of Alzheimer's are experimental. The presenilin proteins 1 and 2 (PS1 and PS2) interact with the calcium release receptor, the IP3R, in the endoplasmic reticulum. The mutant forms of the protein increase the activity of the IP3R, thus increasing calcium levels in cells. The team observed in their mice experiment that the reduced expression of IP3R1 decreased amyloid plaque accumulation in brain tissue and the buildup of tau protein, which are characteristics of advanced Alzheimer's disease. The team's results indicate that the IP3 signaling pathway could be a potential medicinal target for patients that have the mutations in presenilins linked to Alzheimer's. Foskett says that even though the assumption is that FAD is just an earlier, more aggressive onset of AD, no one really knows if the causation of FAD is the same to the common AD. The team's findings is important to find effective treatments that target the IP3R and calcium signaling, specifically for the FAD patients.
Connection:
This article connects to our class' study about the nervous system and its related diseases. Homeostasis is the process by which organisms maintain a relatively stable environment. Alzheimer's disease creates homeostatic imbalance with part of the nervous system's function, starting with the hippocampus and affecting memory. It can spread to all parts of the brain, further inhibiting normal nervous system actions. Even though Alzheimer's disease is the 6th leading cause of death in the US, there is no known cure for it. This relates to the article because their study shows a possibility of a way to prevent the restriction on the nervous system's major functions. The article describing Foskett's team's experimental findings offers an idea for new treatments regarding FAD, a more recurrent version of AD with similar symptoms. The team, by testing on mice with similar FAD-causing mutation presenilins, may be able to use their research to find treatments that will be able to help maintain homeostasis in the nervous system for people with FAD.
Did the experimental treatments have any noticeable side effects on the mice? Are there any dangers of using the experimental treatment?
ReplyDeleteThe experiment did not discover any exact treatments, but more of ideas for future treatments. The noticeable side effects on the mice based on the team's experiment were the amyloid plaque and buildup of tau protein. These side effects support the team to show that the presenilin proteins affecting the calcium levels in cells in turn affect these Alzheimer's-like conditions in the mice. There are no dangers of using the experimental treatment because there isn't a true treatment as of now, just possibilities of what treatments could be used based on these proteins' role.
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