Three stories, the first more interesting, the next two much better than all the other depressing stuff smothering the news. (None of these are up-to-the-minute. I’ve been offline, not to say out of it, for a while.)
(J. Pathol., abstract, and ScienceDaily.) Professor Ruth Itzhaki and her team at the University [of Manchester’s] Faculty of Life Sciences have investigated the role of herpes simplex virus type 1 (HSV1) in [Alzheimers Disease] ….
Most people are infected with this virus, which then remains life-long in the peripheral nervous system, and in 20-40% of those infected it causes cold sores. Evidence of a viral role in AD would point to the use of antiviral agents to stop progression of the disease.
The team discovered that the HSV1 DNA is located very specifically in amyloid plaques: 90% of plaques in Alzheimer’s disease sufferers’ brains contain HSV1 DNA, and most of the viral DNA is located within amyloid plaques. The team had previously shown that HSV1 infection of nerve-type cells induces deposition of the main component, beta amyloid, of amyloid plaques. Together, these findings strongly implicate HSV1 as a major factor in the formation of amyloid deposits and plaques, abnormalities thought by many in the field to be major contributors to Alzheimer’s disease.
This is a major breakthrough against Alzheimers, if the results hold up on further research.
Two huge triumphs, quietly happening:
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