In a study from UT Health San Antonio, scientists found that an inflammatory trigger during viral infections is increased in Alzheimer’s disease and progressive supranuclear palsy, a rare brain disorder.
They found a new trigger of brain inflammation in these disorders.
Alzheimer’s disease and progressive supranuclear palsy are marked by toxic deposits of a protein called tau.
The current study found that tau-induced “jumping genes”—which can relocate or copy themselves to other locations in the genome—form double-stranded RNA.
This abnormal RNA mimics the inflammatory trigger that is also present in viral infections.
Transposable elements—the so-called jumping genes—are a new area of interest in understanding Alzheimer’s disease.
This study provides new insights into how they can drive the disease process in addition to their ability to jump.
These double-stranded RNAs look like a virus to the immune system even though the jumping genes are a part of our normal genome.
In the study, the researchers detected an accumulation of double-stranded RNA in postmortem brain tissue from patients with Alzheimer’s disease and progressive supranuclear palsy and in the brains of mouse and fruit fly models of tauopathy.
In aging and disease, astrocytes respond to injury and disruption of the neuronal environment. The new findings open new doors for understanding astrocyte biology and its role in transposable element control.
Loss of neurons, which are cells of the central nervous system, is progressive in Alzheimer’s and other neurodegenerative diseases.
The team says they are currently targeting jumping gene activation in a local Phase II clinical trial for patients with Alzheimer’s disease, and it’s important to understand the full repertoire of toxic molecules, including double-stranded RNAs, that jumping genes produce.
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The study was conducted by Elizabeth Ochoa et al and published in Science Advances.
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