Genetic Relics: How Ancient Viral DNA Could Accelerate Neurodegeneration

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Genetic Relics: How Ancient Viral DNA Could Accelerate Neurodegeneration
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Research suggests that endogenous retroviruses within the human genome could influence the development of neurodegenerative diseases by contributing to the spread of abnormal protein aggregates in the brain. Credit: SciTechDaily.comGenetic remnants of viruses that are naturally present in the human genome could affect the development of neurodegenerative diseases. Researchers at DZNE come to this conclusion on the basis of studies on cell cultures. They report on this in the journal.

However, studies indicate that HERV-W is activated in multiple sclerosis and HERV-K in the neurological disease “amyotrophic lateral sclerosis” and in frontotemporal dementia . Now, Vorberg’s team found that the viral proteins facilitate the transport of so-called tau aggregates from cell to cell.

“For the transport of tau aggregates from cell to cell, we see two pathways in particular. Transfer between cells that are in direct contact, and transport within vesicles that act as cargo capsules, so to speak, and pass from one cell to another to eventually merge with it,” Vorberg explained. “In both scenarios, membranes have to fuse. Proteins from the envelope of viruses can promote this process. That’s because many viruses are adapted to fuse with host cells. This happens by means of special proteins that viruses carry on their surfaces. If precisely these proteins are incorporated into the cell membrane and the membrane of extracellular vesicles, it is understandable that the tau aggregates then spread more easily.

Reference: “Reactivated endogenous retroviruses promote protein aggregate spreading” by Shu Liu, Stefanie-Elisabeth Heumüller, André Hossinger, Stephan A. Müller, Oleksandra Buravlova, Stefan F. Lichtenthaler, Philip Denner and Ina M. Vorberg, 18 August 2023,SciTechDaily: Home of the best science and technology news since 1998. Keep up with the latest scitech news via email or social media.

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