>A new paper in Neuron, though, looks to be the most unignorable one yet with evidence that there’s some sort of viral/bacteial/fungal component to the disease. A team led out of a Mt. Sinai research group has gone over a pretty large sample of Alzheimer’s brain tissue (622 patients who died with the disease, and over three hundred control brains as well), sequencing infectious organism DNA, looking for changes in the proteome, etc. They find that aging brains in normal patients display plenty of viral signatures (as indeed is probably the case in many other tissues). But the AD samples were particularly enriched in herpesviruses 6A and 7, a result that repeated across three independent cohorts from different geographical locations (the brain tissue collections were from more than one previous effort). According to Stat, there’s a paper coming out next month from another group entirely that also implicates HHV6.
>A new paper in Neuron, though, looks to be the most unignorable one yet with evidence that there’s some sort of viral/bacteial/fungal component to the disease. A team led out of a Mt. Sinai research group has gone over a pretty large sample of Alzheimer’s brain tissue (622 patients who died with the disease, and over three hundred control brains as well), sequencing infectious organism DNA, looking for changes in the proteome, etc. They find that aging brains in normal patients display plenty of viral signatures (as indeed is probably the case in many other tissues). But the AD samples were particularly enriched in herpesviruses 6A and 7, a result that repeated across three independent cohorts from different geographical locations (the brain tissue collections were from more than one previous effort). According to Stat, there’s a paper coming out next month from another group entirely that also implicates HHV6.