Shingles infection may awaken dormant neurological herpes viruses, causing inflammation and accumulation of Alzheimer’s associated proteins in the brain. Alzheimer’s disease is the most common cause of dementia in older adults and the 7th leading cause of death in the United States, according to
Normally HSV-1 – one of the main variants of the herpes simplex virus — lies dormant within the neurons of the brain. However, when it is activated it leads to the accumulation of tau and amyloid beta proteins and loss of neuronal function. These are signature elements found in patients with Alzheimer’s disease.
When activated, it can cause inflammation in nerves and skin, causing painful open sores and blisters. Most carriers—and according to the CDC that’s one in two Americans—will have between very mild to no symptoms before the virus becomes dormant. The link between HSV-1 and Alzheimer’s disease only occurs when HSV-1 has been reactivated to cause sores, blisters, and other painful inflammatory conditions.To better understand the cause-and-effect relationship between the viruses and Alzheimer’s disease, the Tufts scientists re-createdin small 6-millimeter-wide donut-shaped sponges made of silk protein and collagen.
However, if the neurons already harbored quiescent HSV-1, the exposure to VZV led to a reactivation of HSV, and a dramatic increase in tau and beta-amyloid proteins, and the neuronal signals begin to slow down. The scientists observed that the VZV infected samples started to produce a higher level of cytokines—proteins that are often involved in triggering an inflammatory response. Kaplan noted that VZV is known in many clinical cases to cause inflammation in the brain, which could possibly lead to activation of dormant HSV and increased inflammation.
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