As ugly as cold sores look, the virus behind them may be uglier still. New evidence has supported the growing suspicion of a link between the herpes simplex virus-1 (HSV-1) and Alzheimer鈥檚, especially in people who carry a specific gene variant.
The variant, called ApoE4, is present in about half of all people who develop Alzheimer鈥檚, and around 30 per cent of Caucasians carry at least one copy of it. About 80 per cent of elderly people carry HSV-1, so any exacerbating effect could be having a huge impact. The good news is that antiviral drugs could slow Alzheimer鈥檚 progression in those with HSV-1.
Ruth Itzhaki and colleagues at the University of Manchester, UK, infected cultures of human brain cells with HSV-1 and found that it caused a dramatic increase in levels of amyloid beta protein 鈥� the main constituent of the plaques which form in the brains of people with Alzheimer鈥檚 鈥� within the cells. The team saw a similar increase in the brains of mice that had been infected with HSV-1 (Neuroscience Letters, ). 鈥淭his strongly suggests that the virus produces amyloid protein and, ultimately, plaques in Alzheimer鈥檚 brains,鈥� says Itzhaki.
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In a separate experiment, the team stained brain slices taken from deceased Alzheimer鈥檚 patients and found that DNA from HSV-1 was attached to the amyloid plaques in those people with the virus. The results were presented at the Strategies for Engineered Negligible Senescence conference in Cambridge, UK, in September.
鈥淪lices taken from the brains of deceased Alzheimer鈥檚 patients showed that herpes DNA was attached to the plaques鈥�
鈥淭he new data clearly show that HSV infection directly correlates with increases in the intracellular accumulation of toxic amyloid beta,鈥� says Renee Miller at the University of Rochester Medical Center in New York. But proving definitively that HSV-1 causes Alzheimer鈥檚 may be difficult, she says, as 鈥渢here are likely to be many different routes to the same end state鈥�.
Last year, Miller showed that HSV-1 was more active in mice with ApoE4 than those with other forms of the gene. Itzhaki suggests that in people carrying the variant, HSV-1 is repeatedly reactivated from an otherwise latent state. She now wants to test whether antiviral drugs could 鈥渟witch off鈥� this process. 鈥淚 think there鈥檚 enough evidence to begin giving people with ApoE4 antiviral drugs to slow the progression of the disease.鈥� Ultimately, she says, it may be possible to vaccinate ApoE4-positive people against HSV-1 in childhood.
However, Clive Ballard of the UK鈥檚 Alzheimer鈥檚 Society notes that it is hard to tell how relevant cell-culture work is to the treatment of people with Alzheimer鈥檚.
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