Are fever blisters genetic
Herpes viruses as Alzheimer's triggers?
The evidence is growing: One cause of Alzheimer's dementia could be the herpes simplex virus - the causative agent of cold sores and co. New evidence for this is provided by an experiment with human brain tissue. If these neurons were infected with the herpes virus, amyloid plaques developed, brain cells died and messenger substances typical of Alzheimer's were created, as the researchers report in the journal "Science Advances".
Although Alzheimer's is one of the most common neurodegenerative diseases worldwide, the cause of this dementia is still unknown. Although there are some genetically determined forms of Alzheimer's disease, 95 percent of the cases develop the so-called sporadic form, the cause of which is unknown. Various environmental factors such as fine dust, aluminum and other pollutants are suspected, but also pathogens such as periodontal bacteria or certain viruses.
Herpes virus suspected
One pathogen has come into focus: herpes simplex. After an infection, this virus remains in the body for life and nests in the fine nerve endings of the skin and the nerve fibers that continue. If the pathogens then become active, the typical lip vesicles form, but in rare cases herpes can also penetrate the brain and cause encephalitis there.
Several studies now suggest that there may be a link between herpes viruses and Alzheimer's disease. High densities of these viruses have been found in amyloid plaques in Alzheimer's patients, and researchers in Taiwan have found in an epidemiological study that infection with herpes significantly increases the risk of developing Alzheimer's disease later on. However, it remained uncertain whether there was a causal connection.
Virus attack creates amyloid plaques and tau proteins
Dana Cairns from Tufts University in Massachusetts and her team have now investigated this more closely. For their study, they used neuronal stem cells to grow two- and three-dimensional tissue cultures of human brain cells. In the 3D cultures, the cells grew on a ring-shaped scaffold made of silk protein and formed layers similar to those of the gray and white brain matter in the adult brain. The researchers then infected these tissue cultures with herpes simplex and watched what happened.
“The results were amazing,” says Cairns colleague David Kaplan. "Only three days after the herpes infection, large, dense plaques made of beta-amyloid formed and the enzymes that promote this plaque formation were also increasingly released." A special staining of the tissue also revealed that the dew that is typical of Alzheimer's disease also developed -Enriched proteins. At the same time, the virus attack changed the gene activity of the neurons: the researchers found that 40 genes associated with Alzheimer's disease were clearly overactivated, they report.
Indication of causal relationship
All of this had fatal consequences for the brain cells: one week after the infection, extensive areas with dead brain cells were visible in the tissue model, as the researchers report. "We observed the loss of neurons, as well as inflammation of the tissue and suppressed communication between the brain cells - exactly what we also see in Alzheimer's patients," reports Kaplan.
According to Cairns and her team, these results suggest that there is a causal link between herpes infection of the brain and Alzheimer's disease. "This is the first study that demonstrates so many physiologically relevant features of the disease in a model system," say the scientists. "Our three-dimensional tissue model of the brain shows that the herpes virus alone is enough to trigger typical Alzheimer's symptoms."
Antiviral agent prevents degeneration
This is supported by a second experiment. In this, the researchers treated the infected tissue cultures with valaciclovir, a drug often used against herpes viruses. “We wanted to know if inhibiting the virus with this antiviral could also reduce the Alzheimer's-like characteristics,” explain Cairns and her team.
And indeed: the neuronal tissues that were given a dose of valaciclovir immediately after infection with the herpes virus did not develop any amyloid plaques and the production of Alzheimer's-typical enzymes and messenger substances remained normal. In the tissues that had received the antiviral agent only one day after infection, the pathological changes were at least reduced compared with the controls.
“That could mean that this type of pharmaceutical intervention could also be useful in preventing or treating Alzheimer's disease in patients,” say Cairns and her colleagues. Further studies must now investigate this. (Science Advances, 2020; doi: 10.1126 / sciadv.aay8828)
Source: Tufts UniversityMay 7, 2020
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