Structural Biochemistry/Transgenic Animal

Overview
Transgenic animal are animals that have had foreign genes from another animal introduced into their genome. A foreign gene (such as a hormone or blood protein) is cloned and injected into the nuclei of another animal’s in vitro fertilized egg. Cells are then able to integrate with the transgene, and the foreign gene is expressed, upon which the developing embryo is surgically implanted in a surrogate mother. The result of this process, if the embryo develops, is a transgenic animal housing a particular gene from another species.

Applications of transgenic technology are for example, improving upon livestock, such as higher quality wool in sheep, or increasing the amount of muscle mass of an animal so that it can produce more meat for consumption. Conversely, transgenic animals can also be utilized for medical purposes such as producing human proteins by inserting a desired transgene into the genome of an animal in a manner that causes the target protein to be expressed in the milk of the trangenic animal.

The expression of a transgene can also be engineered to take place in plants, such as obtaining the bio-luminescent gene that gives fireflies their glow in the dark ability, and introducing it to a plant.

Transgenic Mice in Alzheimer's Research
Recently, transgenic mice have been used to conduct research concerning Alzheimer’s Disease. Researchers have created a new transgenic mouse that carries the gene for human Alzheimer’s disease, which represents a breakthrough in the development of effective treatments for a currently incurable disease. Researchers developed these transgenic mice by harvesting DNA that activate genes in the brain affected by the disease, including the hippocampus and cerebral cortex. This DNA was then inserted into mice embryos via microinjection techniques. This new DNA then became part of the mouse’s genotype through hybridization of this foreign DNA with the mouse’s own DNA.

Observable results in the brains of the mice were not seen within the first six months of life, but between six and nine months, the transgenic mice developed similar characteristics as ones seen in human Alzheimer’s patients. Such changes include damage to the neurons in the brain, reduction in synapse density, and accumulation of pathogenic beta-amyloid deposits. These beta-amyloid deposits increased in size as the mice aged and reached levels proportional to the amount of deposits that develop in human Alzheimer’s patients. The development of the amyloid plaques have been shown in transgenic mice to have adverse affects on memory, which resemble memory deficits seen in human patients.

The Morris water maze is a test conducted on transgenic mice demonstrating the memory loss  resulting from damage to the hippocampus. This test involves placing a mouse inside a shallow pool of water that contains a submerged platform, which remains out of site of the mouse for the duration of the test. The mouse is placed in the pool on the opposite of the platform and is allowed to find the submerged platform by swimming around the pool and using visual cues on the surrounding walls. The test is performed multiple times and each time the mouse is placed in the same pool, the time spent swimming around in search of the platform decreases, which is a result of the formation of memories the mouse has stored of the various cues. The Alzheimer’s transgenic mice perform poorly when subjected to this same test, which indicates significant damage to their hippocampus: the location of memory storage in the brain.

One of the main reasons for developing these transgenic mice is to determine whether or not these harmful amyloid plaques are the cause for Alzheimer’s Disease, and what types of treatment can be developed to prevent them from forming and/or limit their growth. These transgenic mice not only provide more insight into the cause of Alzheimer’s but they also function as models for testing drugs to treat the disease.

More transgenic animals: ,

Resources
http://www.accessexcellence.org/WN/SUA02/alzheimers_breakthrough.php