“Jumping” Inflammatory Trigger Plays a Key Role in Alzheimer’s Disease Progression
Study provides new insights into how neuroproteins interact with genomic elements to affect the progression of Alzheimer's disease.
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“Jumping” Inflammatory Trigger Plays Key Role in Alzheimer’s Progression

Experiments in humans and fruit flies link “jumping” trigger to neurodegeneration

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Swathi Kodaikal, MSc

Swathi Kodaikal, MSc, holds a master’s degree in biotechnology and has worked in places where actual science and research happen. Blending her love for writing with science, Swathi enjoys demystifying...

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Published:Jan 17, 2023
|2 min read

According to new research, a novel inflammatory trigger has been found to be elevated in Alzheimer’s disease and progressive supranuclear palsy. Researchers from UT Health San Antonio have reported that tau-induced “jumping genes” form double-stranded (ds) RNA, which is abnormal and flares up systemic inflammation the way a dsRNA virus would.  

What are jumping genes?

Jumping genes, also known as transposable elements, are sequences of DNA that move (or jump) from one location in our genome to another. Once disregarded as “junk” DNA, these elements are now being investigated and linked to key regulatory and evolutionary roles.

Tau is a phosphoprotein found in the normal adult brain. In those with brain diseases like  Alzheimer’s and progressive supranuclear palsy, tau protein gets hyperphosphorylated and deposited as toxic aggregates in the neuronal network. This latest study provides new insights into how tau deposits interact with jumping genes and jointly drive the disease process.

“Transposable elements are a new area of interest in understanding Alzheimer’s disease,” said Elizabeth Ochoa, PhD, first author of the paper, in a recent press release. “These dsRNAs (copied from our DNA) look like a virus to the immune system even though the jumping genes are a part of our normal genome.” 

“We found substantial deposits of dsRNA in astrocytes, which are cells that provide metabolic support for neurons, regulate neurotransmitters, and maintain blood-brain barrier integrity,” said Bess Frost, PhD, the senior author and Ochoa’s mentor. “Our findings open new doors for understanding astrocyte biology and [its] role in transposable element control.”

Supported by the National Institute of Neurological Diseases and Stroke, the Rainwater Charitable Foundation, and the National Institute of General Medical Sciences, the team is targeting jumping gene activation in a local Phase 2 clinical trial for patients with Alzheimer’s disease. The researchers aim to better understand the full repertoire of toxic molecules produced by jumping genes.