Studies say proteins are essential for all biological activities and the health of the cell.
Misfolded and damaged proteins spell trouble and are common to all human neurodegenerative diseases and many other age-associated diseases.But when during a lifespan do proteins start to misbehave?
A new Northwestern University study reports that protein damage can be detected much earlier than we had thought, long before individuals exhibit symptoms. But the study also suggests if we intervene early enough, the damage could be delayed.
In studying seven different proteins of the worm C. elegans, the researchers discovered that each protein misfolds at the same point: during early adulthood and long before the animal shows any behavioral, or physiological, change. (Each protein had a minor mutation that affects folding.)
The misfolding coincided with the loss of a critical protective cellular mechanism: the ability to activate the heat shock response, an ancient genetic switch that senses damaged proteins and protects cells by preventing protein misfolding.
The results will be published online during the week of Aug. 24 by the Proceedings of the National Academy of Sciences (PNAS).
"I didn't expect the results to be so dramatic, for these different proteins that vary in concentration and are expressed in diverse tissues to collapse at the same time," said lead researcher Richard I. Morimoto. "This suggests the animal's protective cellular stress response becomes deficient during aging."
Could the damaging events of protein misfolding be prevented or at least delayed?