Antiviral drugs used to target the herpes virus could be effective at slowing the progression of Alzheimer’s disease (AD), a new study shows.
The University of Manchester scientists have previously shown that the herpes simplex virus type 1 (HSV1) is a risk factor for Alzheimer’s when it is present in the brains of people who have a specific genetic risk to the disease.
AD is an incurable neurodegenerative condition affecting about 18 million people worldwide. The causes of the disease or of the abnormal protein structures seen in AD brains – amyloid plaques and neurofibrillary tangles – are completely unknown.
The Manchester team has established that the herpes virus causes accumulation of two key AD proteins – β-amyloid (Aβ) and abnormally phosphorylated tau (P-tau) – known to be the main components of plaques and tangles respectively. Both proteins are thought by many scientists to be involved in the development of the disease.
“We have found that the viral DNA in AD brains is very specifically located within amyloid plaques,” said Professor Ruth Itzhaki, who led the team in the University’s Faculty of Life Sciences. “This, together with the production of amyloid that the virus induces, suggests that HSV1 is a cause of toxic amyloid products and of plaques.
Antiviral drugs used to target the herpes virus could be effective at slowing the progression of Alzheimer’s disease (AD), a new study shows.
The University of Manchester scientists have previously shown that the herpes simplex virus type 1 (HSV1) is a risk factor for Alzheimer’s when it is present in the brains of people who have a specific genetic risk to the disease.
AD is an incurable neurodegenerative condition affecting about 18 million people worldwide. The causes of the disease or of the abnormal protein structures seen in AD brains – amyloid plaques and neurofibrillary tangles – are completely unknown.
The Manchester team has established that the herpes virus causes accumulation of two key AD proteins – β-amyloid (Aβ) and abnormally phosphorylated tau (P-tau) – known to be the main components of plaques and tangles respectively. Both proteins are thought by many scientists to be involved in the development of the disease.
“We have found that the viral DNA in AD brains is very specifically located within amyloid plaques,” said Professor Ruth Itzhaki, who led the team in the University’s Faculty of Life Sciences. “This, together with the production of amyloid that the virus induces, suggests that HSV1 is a cause of toxic amyloid products and of plaques.