Science Market Update

U. Alabama Analytical Lab Study Shows Lipid Count Impacts Parkinson’s

Written by Jennifer Nieuwkerk | Fri, Sep 19, 2014

With fundraising campaigns such as the ALS ice bucket challenge in the news, diseases of the nervous system have recently received a great deal of attention from both the media and life science researchers. Parkinson’s disease in particular has been the subject of a recent study at the University of Alabama. Scientists at the university discovered that the deficiency of a type of lipid that naturally declines as the brain ages leads to increases in a protein associated with Parkinson’s disease.

 “This gets right to the heart of understanding, possibly, the mechanism by which one form of lipid is impacting the process of neuron degeneration,” said Dr. Guy Caldwell, UA professor of biological sciences and one of the study’s co-authors.

Dr. Caldwell works with other life science researchers at the University of Alabama to study malfunction in basic cellular mechanisms as it relates to diseases of the nervous system. His analytical lab uses microscopic nematode roundworms to study gene function and therapeutic target development for nervous system disorders. Caldwell and his research team were the first to apply this model in the study of several disorders including dystonia, Parkinson’s disease and epilepsy. His team also focuses on Alzheimer’s disease, ALS and cystic fibrosis.

 

Dr. Caldwell

Image courtesy of University of Alabama

 

In the Parkinson’s study, researchers focused on how low levels of phosphatidylethanolamine, a type of lipid known as PE, can lead to high levels of alpha-synuclein, a protein associated with Parkinson’s. Studies in the past have suggested that excess alpha-synuclein can work as an intra-cellular “roadblock” that stops proteins and dopamine from being transported to their necessary locations. Serious disorders can be the result of this disruption in delivery.

“That situation is being applied here, but in a different way,” Caldwell said. “We’re gaining a better understanding of the importance these lipids, which are components of cellular membranes, have in maintaining proper trafficking.”

Using yeast and the nematode C. elegans in their analytical lab, the researchers showed they could solve the delivery problem by adding doses of a second lipid, ethanolamine, or ETA.

“This supplementation of ETA basically tells us that if we can restore the amount of PE that is being made, we can create a healthier situation in neurons, and this might help them to survive longer.”

Dr. Caldwell said more research with rodents and patient-derived stem cells is needed to know whether this treatment could eventually prove beneficial in humans. One day, though, it’s possible that a supplement could be developed to prevent the decline of PE or a drug may be created with the potential to activate an enzyme that converts ETA to PE. There’s a long way to go in creating better treatments for Parkinson’s disease, but this study is a significant discovery along the way.

Funding for this type of research is abundant at the University of Alabama. So far in 2014, the National Institutes of Health has given the University of Alabama, Birmingham $170.1 million in research funding. The University of Alabama  is also known worldwide for its quality research and advanced scientific findings. Ranked among the top 50 public universities in the nation in U.S. News and World Report’s annual college rankings for over ten years, the University of Alabama ranked 32nd among public universities in the 2013 rankings.

If you would like to meet face-to-face with life science researchers in Alabama working to stock their analytical lab with quality supplies, Biotechnology Calendar, Inc. invites you to exhibit at the BioResearch Product Faire™ Event at the University of Alabama  on November 13th, 2014. For more BCI show dates across the country, see the 2014 calendar of events. Research funding statistics for the University of Alabama as well as additional vendor show information is available when you click on the button below.