@DrShawnL Hey - b/c they have shown that amyloid beta appears to actually be an antimicrobial peptide that - at least in the lab/mice - forms in response to a range of bacterial, viral + fungal pathogens capable of persisting in the CNS, including the herpesviruses: ncbi.nlm.nih.gov/pmc/articles/P… 
@DrShawnL 2/ Related studies by team’s like @G_Tetz support their findings. Here Tetz found that, in the lab, Tau formation may be additionally promoted by DNA from bacterial pathogens like Borrelia: nature.com/articles/s4159…
@DrShawnL @G_Tetz 3/ Meanwhile herpesviruses have been identified in human Alzheimer’s autopsied brains + shown capable of driving neuroinflammation (cell.com/neuron/pdfExte…) So has oral pathogen p. gingivalis and the toxic gingipains proteins it produces (advances.sciencemag.org/content/5/1/ea…)
@DrShawnL @G_Tetz 4/ If you take just the pathogens I mentioned above (b/c there are likely other less-studied polymicrobial contributors)..rates of #Borrelia infection as evidenced by Lyme cases are skyrocketting. Herpesvirus spread in the early in teens is also very high: google.com/amp/s/www.nbcp…
@DrShawnL @G_Tetz 5/ Then consider that a growing number of young patients, especially in the USA, are being aggressively prescribed immunosuppressive drugs like Humira that impair the immune system’s ability to manage Alzheimer’s-associated and related pathogens: microbeminded.com/2018/03/31/ant…
@DrShawnL @G_Tetz 6/ Then, we are failing to adequately study how Alzheimer’s-related pathogens may be passed by mother to child in the womb. For example, CDC admits Borrelia congenital transfer, but the topic is barely studied (although here’s one example): ncbi.nlm.nih.gov/pmc/articles/P…
@DrShawnL @G_Tetz 7/ So to summarize my top 4 factors: 1. Lack of widespread acceptance of studies indicating pathogen activity in #Alzheimer’s 2. Increased spread of such pathogens during that same period 3. Increased use of immunosuppressive drugs 4. Failure to study congenital pathogen transfer
