Neurodegenerative disease marked by amyloid-beta plaques and tau tangles. mTOR overactivation blocks the autophagy that would clear these toxic proteins; rapamycin restores clearance in mouse models.
| Tier | What it means | Studies |
|---|---|---|
| C | Animal in vivo | 3 |
No direct human evidence in the Atlas for this entity yet — everything below rests on animal or mechanistic work.
| Study | Year | Tier | Finding |
|---|---|---|---|
| BAB2025 | 2026 | C | UPDATE (was bioRxiv preprint at seed time, peer-reviewed and published in Advanced Science March 2026). Restricting individual branched-chain amino acids has distinct, sex-specific effects on cognitio |
| CAC2010 | 2010 | C | Revealed a vicious cycle: amyloid-beta RAISES mTOR activity, and high mTOR in turn blocks the autophagy needed to clear amyloid and tau - so the disease feeds itself. Rapamycin broke the loop in 3xTg- |
| SPI2010 | 2010 | C | Connected the longevity drug to a specific age-related disease. Long-term rapamycin prevented memory deficits and lowered toxic amyloid-beta in an Alzheimer's mouse model - and the benefit tracked wit |