Can antivirals slow down Alzheimer's? Scientists seek answers

For years, researchers have blamed amyloid and tau proteins for being the main villains behind Alzheimer's. These proteins formed plaques and tangles in the brain, wreaking havoc on neurons. However, recent research on herpes zoster has strengthened an alternative theory: that viruses could trigger the disease.

Ruth Itzhaki, a pioneer in this field, has argued for nearly four decades that the herpes simplex virus 1 (HSV1) could be behind Alzheimer's. Although it sounds like science fiction, her experiments show that HSV1 infection increases amyloid levels in brain cells. A real revelation!

Some critics argued that the viral theory did not fit with the strong genetic component of Alzheimer's. But what if the amyloid and tau proteins were actually the brain's defense against pathogens, as suggested by William Eimer from Harvard?

In small amounts, these proteins could be beneficial. But if the immune system becomes overwhelmed, they could aggregate and form the harmful plaques and tangles. It's as if the brain is fighting an internal battle against invisible invaders.

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The finding that vaccination against herpes zoster could protect against dementia has left many astonished. Who would have imagined it? This discovery could explain why people with Down syndrome, who produce more amyloid protein, are more prone to Alzheimer's. Furthermore, individuals with a genetic variant called ApoE4 are more vulnerable, but only if they have HSV1 in the brain. It's as if the virus and genetics are conspiring together!

It has even been found that the reactivation of HSV1 can be triggered by another pathogen, the herpes zoster virus. This could be the reason why the herpes zoster vaccine offers protection. And surprise, surprise, a traumatic brain injury could also awaken dormant HSV1 and initiate the formation of plaques and tangles.

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