With their bright colors and tendency to school, zebrafish are commonly found in home aquariums.
Scientists, however, are interested in this tiny fish for a medical reason… the zebrafish present an ideal model to study human genetic diseases like Alzheimer’s disease.
Now, new research using zebrafish reveals a trigger for Alzheimer’s disease that could one day result in better prevention and treatment.
When it comes to studying genetic illnesses, many researchers choose rodents. Rodent studies allow scientists to determine if a mutation in a specific gene can cause a given illness in humans, but recent results using zebrafish show this aquarium staple may be an even better model.
This is because zebrafish share most human body parts and organs, and a whopping 70 percent of our genes. This means diseases that affect these shared body parts—like the brain— can be easily modeled in the fish.
Other advantages of using zebrafish in medical science include ease of breeding and their ability to produce up to 300 eggs. These eggs are laid and fertilized externally, allowing them to be readily manipulated. What’s more, these large families make it easier for scientists to detect subtle genetic effects among offspring.
Human diseases that have been successfully modeled in the zebrafish include Duchenne muscular dystrophy and skin cancer (melanoma). Recently, Australian researchers turned to Alzheimer’s disease and made a surprising finding.
Disrupted Oxygen Generation
The University of Adelaide team analyzed young adult (pre-disease) brains of zebrafish that had gene mutations linked to early-onset Alzheimer’s.
The researchers used cutting-edge technology and mathematical analysis to compare differences in brain cells’ gene activity in normal fish compared to those with mutations. Although different mutations impact brain cell functions in a variety of ways, mutations in Alzheimer’s disease all affected one key function – the use of cellular oxygen to create energy.
The researchers published their paper in the journal Disease Models and Mechanisms in January, writing, “We identify changes to energy metabolism as the earliest detectable cellular stress due to Alzheimer’s disease mutations.”
Lead researcher Dr. Karissa Barthelson, from the University’s Alzheimer’s Genetics Laboratory, explained, saying, “This is very interesting because we know when Alzheimer’s disease eventually develops, people’s brains become severely deficient in energy production.
“When we realized this common link, we took our research one step further and re-analyzed data from another research group that had studied an important Alzheimer’s disease gene in mice.
“We could see a similar effect, and this reinforces our confidence that we have found a fundamental, early driver of Alzheimer’s disease in humans.”
What does this mean? Good news…
Alzheimer’s May Become Easier to Prevent and Treat
Since the brain has many different cell types that produce and share energy in different ways, the Adelaide researchers want to carry out further studies to examine these differences.
“It is very satisfying to have found this important common, early factor driving the development of Alzheimer’s disease,” Dr. Barthelson continued.
“Energy production is the most fundamentally important cellular activity supporting all other functions, particularly in highly active organs such as brains.
“If we can understand in detail what is going wrong with oxygen use and energy production, we may see ways of stopping the disease before it starts.”
