Alzheimer's disease causes loss of normal amyloid-beta protein
What is it about?
Proteins can function when in their normal, soluble state, and cease to function when in any other state. The official narrative has been that when proteins become aggregated, they turn toxic. But a review of data in humans affected by Alzheimer's disease, the most common neurodegenerative disorder, the problem is that amyloid-beta, a key protein for normal brain health, depletes as it transforms into amyloid, cross-beta sheets of stable, non-functioning protein.
Why is it important?
We reviewed data to show that the problem in neurodegeneration is the loss of normal protein rather than its accrual into "toxic proteinopathy." This opens a completely different therapeutic strategy: replacing normal protein to levels above a compensation threshold. This would represent a major departure from the decades-old approach to Alzheimer's and other neurodegenerative disorders, centered on anti-amyloid approaches, which have yielded futility or harm.