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All neurodegenerative diseases have a common thread: the appearance of protein clumps in the brain such as amyloid-beta plaques in Alzheimer's disease and alpha synuclein aggregates in Parkinson's. The root cause of this buildup has been hard to pinpoint, but Rockefeller scientists have identified a likely culprit that opens up a new avenue for developing treatments.
In a pair of studies carried out in flies and mice, the researchers discovered that the issue lies in the system that transports proteasomes, the molecular machinery that breaks down proteins, to specific locations within a cell.
[...] "This is the first study to find a mechanism by which the proteasomes are moved to nerve endings to do their job," says Hermann Steller, the Strang Professor at Rockefeller. "When this mechanism gets disrupted, there are severe consequences for the function and long-term survival of nerve cells."
Proteasomes are made in the cell body of a neuron and need to be transported over long distances to reach the nerve endings where the neuron connects with other cells--a journey of more than one meter in some cases. When proteasomes fail to reach these critical communication hubs, the cell descends into turmoil.
"Instead of being degraded, damaged proteins in these sites hang around long enough to interact with other binding partners, form aggregates, and disrupt cell function," Steller says. Over time, this causes degeneration of nerve fibers and ultimately cell death.
When Steller and his team began investigating the proteasome transportation system in fruit flies, they identified a protein called PI31, which plays a crucial role in loading the proteasomes onto the cellular components that ferry them around. In research published in Developmental Cell, they show that PI31 enhances binding and promotes movement of proteasomes with cellular motors. Without it, transport is halted. This is the case in both fly and mouse neurons, suggesting that the transport mechanism is common between many species.
(Score: 0) by Anonymous Coward on Wednesday December 11 2019, @12:31AM (3 children)
This is getting kind of tiring, I'm already eating fiber, anti-oxidants and a variety of other "super foods. I guess we need to know what are the precursors to PI31?
Are there organic foods I can eat that include them?
(Score: 2) by Hartree on Wednesday December 11 2019, @12:42AM (1 child)
No, no. The right reaction isn't to actually eat them yourself. It's to over-promote them and sell them to the suck... I mean, health conscious consumers. Yeah. That's the ticket.
(Score: 0) by Anonymous Coward on Wednesday December 11 2019, @03:45AM
> Over time, this causes degeneration of nerve fibers and ultimately cell death.
If I get rich (selling to suckers), will that help stave off this degeneration? Or will getting rich make me a degenerate??
(Score: 2) by HiThere on Wednesday December 11 2019, @04:29AM
Sorry, but that thing about anti-oxidants was someone overreading the results of a few experiments. The anti-oxidants actually *do* prevent a few problems, but dosage is a critical problem, and most people with healthy diets don't need them. Also, too many anti-oxidants interferes with the body's infection fighting mechanism. Whoops!
Everyone wants these things to be simple, but generally in biology if you have a simple answer, it's wrong.
Javascript is what you use to allow unknown third parties to run software you have no idea about on your computer.