Misleading headline. What they actually demonstrated is reversing amyloid accumulation and the cognitive deficits in a transgenic mouse whose pathology is essentially just amyloid accumulation. Calling that “reversing Alzheimer’s” treats amyloid buildup and the disease as the same thing, which is exactly the conflation the amyloid hypothesis has been criticised for over the last decade.
Alzheimer’s in humans is amyloid + tau tangles + neuroinflammation + vascular dysfunction + actual neurodegeneration (entorhinal and hippocampal neurons dying, brain volume measurably dropping on MRI). Tau burden correlates with cognitive decline far better than amyloid does. The IBEC paper addresses one of those layers, the upstream-ish one, in a model that doesn’t reproduce most of the others. Fixing a cause in a young system before damage has accumulated is just not the same operation as fixing an established disease in an old human cortex that’s already lost the cells.
The human translation data backs this up. Lecanemab clears plaques and slows cognitive decline by about 27% over 18 months. Donanemab clears around 76% of plaques and slows decline by ~35% in early AD. In both trials both arms still declined, treatment just declined a bit more slowly. Northwestern’s Mesulam Institute puts it bluntly: “These medications do not reverse existing disease or stop the progression.” So removing amyloid in a system that already has the full human pathology bends the curve, it doesn’t undo anything.
What the IBEC team has here is a genuinely interesting result for the cerebrovascular angle, where BBB dysfunction and glymphatic clearance failure are upstream of plaque accumulation rather than a downstream consequence. The LRP1 transport mechanism and the multivalent ligand design are clever and well-grounded. The fair claim is “we improved amyloid clearance and rescued behavioural deficits in an amyloid-overexpressing mouse by targeting BBB transport.” That’s a real contribution. “Reversed Alzheimer’s” sells the mechanism by overstating what it did, and it sets up the same disappointment cycle the field has been through with every other anti-amyloid intervention that worked great in mice.
Original paper, for anyone wanting the actual data: https://doi.org/10.1038/s41392-025-02426-1
The amyloid hypothesis has been supported by fraud for 20 years.
Pharma made drugs that dropped amyloid by 30% and they do NOTHING despite FDA approvals.
Mouse models do not get dementia.
The amyloid hypothesis has been supported by fraud for 20 years.
Pharma made drugs that dropped amyloid by 30% and they do NOTHING despite FDA approvals.
Okay, got any sources for that, or should we take you at your word?
Mouse models do not get dementia.
I don’t believe I said they did. Why the confrontational tone?
It is a destructive disease so true reversal is not possible, brain capacity might be restored but memories and prior connectivity generally once lost is gone forever.
If catched early enough, that could save some memories before they’re destroyed
And as the long term effects, at least in mice, look promising, I’m kinda hopeful
Was absolutely awful watching my grandmother decline - and because of that, my mother is horrifically afraid of getting dementia
I hope this can translate from mice to humans fast and we can get something similar.
Restoring destroyed neurons will probably never be possible…
But at least we can stop the decline and new memories can be stored again, and with that a kinda normal lifeSorry to hear about your grandmother, but all NIH research on this was halted in 2025 and that was 80% of worldwide efforts.
Governments do not care, anywhere.
Ah, well … Shit
I thought it was mostly a jamming type effect. The memories are often still here, but become progressively less accessible. They then degrade from lack of use.
It might well be that a lot of memories still exist for longer than it seems. Even if not, stopping the degradation, and allowing new memories to form would allow people to remain cognitive and functional for a LOT longer.
For all forms of neurodegeneration, once the cascade starts, it cannot be stopped.
In 2008, a proper controlled imaging study proved that whether there are amyloid plaques in brain or not does not correlate with dementia. 18 years later, people are still spinning in circles with these terrible mouse models.
