Animal Model of Disease
Shirley, New York
(PRLEAP.COM) August 31, 2015 - A team led by Creative Animodel, found that change of developmental mechanisms is the most influential reason in the Parkinson disease. They also explained most damages can be made in the course of these neurons, which causing the death of the function. This work has been done with 4 years, including a delicate project for manipulating mouse genes, to create a unique disease model.
Parkinson Disease (PD) is an incurable neurological disease with the typical symptom of simple tremor, the loss of motor function and cognitive dysfunction and dementia or death in the end. These symptoms are caused by the dopamine (DA) neurons which are mainly controlled for autonomous movement and regulation of emotion.
However, it is always a mystery to wipe out all the neurons in Parkinson's disease. Dopamine neurons in patients often contain strange protein clumps, called Lewy bodies. However, it is not clear whether these clumps cause the death of neurons, or because these neurons themselves attempt to deal with a severe functional disorder by decomposing and re-utilizing the error folding and the functional breakdown of the protein.
Creative Animodel studied Lmx1a and Lmx1b, a pair of closely related transcription factors. These two transcription factors are critical to the development of the neurons, and exist even after the maturation of neurons. In order to study the role of them in mature neurons, the researchers had used the knockout mouse service that can knock down the Lmx1a/b gene only in the dopamine neurons, and at the time they had chosen.
"When we observe the dopamine neurons short of the Lmx1a/b gene, a lot of neurons in the adult mouse appear the same exceptions as Parkinsont in a different period of time. "Creative Animodel said, "the nerve fibers stretching from these neurons degenerate, like nerve endings. "Further more, these knockout mice also show a poor memory and action control in behavioral tests, both of which were Parkinson's symptoms.
By the lysosomal autophagy, cells can break down proteins that are not normally folded so that these molecules do not have a toxic effect on cells. But this process is damaged in Parkinson.
The young mice are given a compound to promote autophagy, which reverse the nerve recession caused by Lmx1b deficiency. In short, the study suggests that the loss of Lmx1b expression is likely to be associated with the pathogenesis of Parkinson. It causes a decline in the function of dopamine neurons, which has gradually weakened and killed the dopamine neurons.
About Creative Animodel
Creative Animodel is now using this unique mouse model to study the role of Lmx1b in the regulation of autophagy. They are also studying the way to prevent Lmx1b deficiency in Parkinson. For more information, please go to our website at http://www.creative-animodel.com/.
CONTACT INFORMATION
Andrea Brook
1-631-372-1052
http://health.einnews.com/article/283892400/1TGbSaMFVkqituI1
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