In a new study, researchers found a possible causal link between sporadic Alzheimer’s disease and herpes simplex virus I infection (HSV-1).
They used a three-dimensional (3-D) human tissue culture model mimicking the components and conditions in the brain to demonstrate the link.
The finding will allow for further studies into the causes and possible treatments of this devastating brain disease.
The research was done by Engineers and scientists led by Tufts University.
Treatment of the brain tissue models with the antiviral drug valacyclovir resulted in reduced plaque formation and other markers of the disease.
Studies by other researchers have implicated pathogens as environmental agents possibly causing the development of Alzheimer’s disease, with a number of studies pointing to HSV-1.
In the study, the team’s brain tissue model allowed them to take a closer look at the potential causal relationship between herpes and Alzheimer’s disease, and the results were intriguing.
After infecting neurons in the bioengineered brain model with HSV-1, the team observed the formation of amyloid plaques, neuronal loss, neuroinflammation, and diminished neural network functionality, all typical features of Alzheimer’s disease.
After just 3 days of herpes infection, they saw large and dense plaque formations of beta-amyloid protein, as well as increased expression of some of the enzymes responsible for generating the plaques.
They observed neuron loss, neuroinflammation, and depressed signaling between neurons—everything we observe in patients.
The researchers found that 40 Alzheimer’s-associated genes were over-expressed in the HSV-1 infected brain tissue constructs compared to non-infected tissue.
Prominent among them were genes coding for the enzymes cathepsin G and BACE2, both known to be linked to Alzheimer’s disease and involved in the production of beta-amyloid peptides found in plaques.
Some of these overexpressed gene products observed in the tissue model could become targets for future drug candidates.
Valacyclovir, which mitigated Alzheimer’s disease-like features in the brain tissue model, is an FDA approved anti-viral medication used to treat herpes infections.
The drug also reduced expression back to pre-infection levels of several molecules and enzymes linked to Alzheimer’s disease, such as presenilin-1.
The lead author of the study is David Kaplan, Stern Family Professor of Engineering and chair of the Department of Biomedical Engineering at Tufts’ School of Engineering.
The study is published in Science Advances.
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