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Hundreds of reports since the 1980s have associated Alzheimer disease with bacteria and viruses. But researchers could not explain the connection. Now new research suggests that viral species, particularly herpes viruses, play a role in Alzheimer disease biology.
The hypotheses that link viruses to brain disease are not new, Richard Hodes, MD, director of the National Institute on Aging, says, but this is the first study to provide “strong evidence” based on unbiased approaches and large datasets.
The study, which was funded by National Institute of Aging (NIA) , originally was intended to find out whether drugs used to treat other diseases can be repurposed for treating Alzheimer. Researchers analyzed large datasets from postmortem brain samples to map and compare biological networks underlying Alzheimer disease. They found that the disease biology is impacted by a “complex constellation” of factors, including the ways the interrelated systems of DNA, RNA, proteins, and metabolites interact with molecular, genetic, and clinical aspects of Alzheimer disease.
Among the key findings: Human herpes virus 6A and 7 were more abundant in Alzheimer disease samples than in non-Alzheimer samples. Researchers also found multiple points of overlap between virus-host interactions and genes associated with Alzheimer risk.
The research “reinforces the complexity of Alzheimer disease,” Hode says, and “highlights the importance of sharing data freely and widely with the research community.”
Hundreds of reports since the 1980s have associated Alzheimer disease with bacteria and viruses. But researchers could not explain the connection. Now new research suggests that viral species, particularly herpes viruses, play a role in Alzheimer disease biology.
The hypotheses that link viruses to brain disease are not new, Richard Hodes, MD, director of the National Institute on Aging, says, but this is the first study to provide “strong evidence” based on unbiased approaches and large datasets.
The study, which was funded by National Institute of Aging (NIA) , originally was intended to find out whether drugs used to treat other diseases can be repurposed for treating Alzheimer. Researchers analyzed large datasets from postmortem brain samples to map and compare biological networks underlying Alzheimer disease. They found that the disease biology is impacted by a “complex constellation” of factors, including the ways the interrelated systems of DNA, RNA, proteins, and metabolites interact with molecular, genetic, and clinical aspects of Alzheimer disease.
Among the key findings: Human herpes virus 6A and 7 were more abundant in Alzheimer disease samples than in non-Alzheimer samples. Researchers also found multiple points of overlap between virus-host interactions and genes associated with Alzheimer risk.
The research “reinforces the complexity of Alzheimer disease,” Hode says, and “highlights the importance of sharing data freely and widely with the research community.”
Hundreds of reports since the 1980s have associated Alzheimer disease with bacteria and viruses. But researchers could not explain the connection. Now new research suggests that viral species, particularly herpes viruses, play a role in Alzheimer disease biology.
The hypotheses that link viruses to brain disease are not new, Richard Hodes, MD, director of the National Institute on Aging, says, but this is the first study to provide “strong evidence” based on unbiased approaches and large datasets.
The study, which was funded by National Institute of Aging (NIA) , originally was intended to find out whether drugs used to treat other diseases can be repurposed for treating Alzheimer. Researchers analyzed large datasets from postmortem brain samples to map and compare biological networks underlying Alzheimer disease. They found that the disease biology is impacted by a “complex constellation” of factors, including the ways the interrelated systems of DNA, RNA, proteins, and metabolites interact with molecular, genetic, and clinical aspects of Alzheimer disease.
Among the key findings: Human herpes virus 6A and 7 were more abundant in Alzheimer disease samples than in non-Alzheimer samples. Researchers also found multiple points of overlap between virus-host interactions and genes associated with Alzheimer risk.
The research “reinforces the complexity of Alzheimer disease,” Hode says, and “highlights the importance of sharing data freely and widely with the research community.”