Proteostasis collapse in aging is a bandwidth problem—not enough chaperones, not excess misfolded proteins

Old cells accumulate protein aggregates. We blame misfolded proteins, but cells have chaperones that handle misfolding perfectly well in youth.

The problem: proteostasis network capacity. Chaperone expression drops with age. UPS activity declines. Autophagy slows.

It's not that more proteins misfold. It's that the cell can't clear them at youth rates. The proteostasis network loses bandwidth, not accuracy.