Abnormal gene copying seen in tauopathy fruit fly models

July 23, 2018

It sounds like science fiction: Nefarious genes clone themselves and settle their rogue copies in distant outposts of the galaxy (namely, our DNA), causing disease.

But it’s a real phenomenon, and in research published July 23, scientists at UT Health San Antonio revealed that this genetic copy-and-paste activity is significantly increased in fruit fly models of tauopathies—neurodegenerative disorders that include Alzheimer’s disease.

The researchers also discovered that lamivudine, an anti-retroviral drug approved for HIV and hepatitis B, decreased the copy-making and reduced the death of neuron cells in the brains of the fruit flies.

This research, published in Nature Neuroscience, suggests a potential novel avenue to treat the memory-robbing disease, which impacts 5.7 million Americans who have an Alzheimer’s diagnosis and the millions more who provide care for them.

The researchers are from the Sam & Ann Barshop Institute for Longevity & Aging Studies, the Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases, and the Department of Cell Systems & Anatomy at UT Health San Antonio.

The team identified “transposable element” activation as a key factor in neuron death in tauopathies. These disorders are marked by deposits of tau protein in the brain. There are more than 20 tauopathies, including Alzheimer’s.

Lamivudine limited expression of genes that make DNA retrotransposons, which are the gene elements that clone themselves and insert the copies into a new spot, said Bess Frost, Ph.D., assistant professor of cell systems & anatomy and member of the Barshop and Biggs institutes at UT Health San Antonio.

Bess Frost, Ph.D.

“We know that these genes are copying themselves at higher levels in the tauopathy fly model,” Dr. Frost said. “And we know we can stop that from happening by giving them this drug.”

It’s thought that the copy-and-paste activity is an effect that follows tau deposit accumulation. Ultimately in the disease course, neurons die.


To read the full article, visit the UT Health San Antonio Newsroom.

Article Categories: News, Research