Blog
Dumbing down, captured or both
A tiresome narrative
Oct 16, 2026
They said that Alzheimer’s disease was due to the buildup of cerebral beta amyloid and p-tau protein. On what was to be nothing more than an assumption, that the buildup of the said proteins caused the neuronal damage and subsequent dementia, billions of dollars have been wasted on developing drugs that decrease these proteins. Even in significant protein clearance the dementia persists and continues its relentless course.
Additionally, perhaps they didn’t notice that many with significant cerebral amyloid never develop dementia!
And then followed blood tests for amyloid and tau … to what end?
Low and behold moves are afoot to develop mRNA-based “vaccines” to prime the immune system against beta amyloid. Seems like no intervention is complete without a “vaccine”!
Am I missing something here?
Somehow this great distraction has precluded them from noticing that folk with mind states devoid of curiosity, meaning and purpose (and a feeling of personal irrelevance) together with degrees of anxiety, disengage and develop dementia. All indications are that the mind states trigger chronic inflammation which underpins the neuro-degeneration.
If this is too complicated for the mechanistic reductionists to comprehend, perhaps they’ll ponder the finding that social isolation increases the risk of developing Alzheimer’s disease by 50%!
It’s clearly a biopsychosocial etiology. And none of your elusive chemicals and “vaccines” have a ghost of a chance of achieving a meaningful outcome.
I would humbly suggest that to rid the world of this scourge (I’m referring to Alzheimer’s disease and not the stupidity of the profession …) rather promote meaningful busyness!
References
Studies of relevance
Cochran review: Decreasing beta amyloid deposits does not improve cognitive loss and/or dementia
https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD016297/full
The existence of beta amyloid deposits in significant amounts is not associated with dementia in many individuals
https://pmc.ncbi.nlm.nih.gov/articles/PMC4486209/
Increased inflammatory activity in the form of chronically raised pro-inflammatory cytokines is associated with increased beta amyloid deposits
https://pmc.ncbi.nlm.nih.gov/articles/PMC6222241/
Persistent stress exposure can contribute to an allostatic load with a predisposition to chronic inflammation
