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July 5, 2018
A Massachusetts General Hospital (MGH) study has found the mechanism by which amyloid beta (A-beta) - the protein deposited into plaques in the brains of patients with Alzheimer's disease—protects from the effects of herpes viruses commonly found in the brain. Along with another study appearing in the same July 11 issue of Neuron, which found elevated levels of three types of herpes viruses in the brains of patients with Alzheimer's disease, the MGH team's results support a potential role for viral infection in accelerating A-beta deposition and Alzheimer's progression.
"There have been multiple epidemiological studies suggesting people with herpes infections are at higher risk for Alzheimer's disease, along with the most recent findings from Icahn School of Medicine at Mt. Sinai that are being published with our study," says Rudolph Tanzi, Ph.D., director of the Genetics and Aging Research Unit in the MassGeneral Institute for Neurodegenerative Disease (MIND) and co-corresponding author of the Neuron paper. "Our findings reveal a simple and direct mechanism by which herpes infections trigger the deposition of brain amyloid as a defense response in the brain. In this way, we have merged the infection hypothesis and amyloid hypothesis into one 'Antimicrobial Response Hypothesis' of Alzheimer's disease."
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A Massachusetts General Hospital (MGH) study has found the mechanism by which amyloid beta (A-beta) - the protein deposited into plaques in the brains of patients with Alzheimer's disease—protects from the effects of herpes viruses commonly found in the brain. Along with another study appearing in the same July 11 issue of Neuron, which found elevated levels of three types of herpes viruses in the brains of patients with Alzheimer's disease, the MGH team's results support a potential role for viral infection in accelerating A-beta deposition and Alzheimer's progression.
"There have been multiple epidemiological studies suggesting people with herpes infections are at higher risk for Alzheimer's disease, along with the most recent findings from Icahn School of Medicine at Mt. Sinai that are being published with our study," says Rudolph Tanzi, Ph.D., director of the Genetics and Aging Research Unit in the MassGeneral Institute for Neurodegenerative Disease (MIND) and co-corresponding author of the Neuron paper. "Our findings reveal a simple and direct mechanism by which herpes infections trigger the deposition of brain amyloid as a defense response in the brain. In this way, we have merged the infection hypothesis and amyloid hypothesis into one 'Antimicrobial Response Hypothesis' of Alzheimer's disease."
Read more