Monday, July 3, 2017

This New Alzheimer's Discovery Could Be The Key To Future Treatments

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Researchers may have uncovered the critical missing piece that could lead to new treatments for Alzheimer’s and other neurodegenerative diseases. It’s an enzyme that plays a role in how the disease develops, but could also be harnessed to work against the tangled accumulation of proteins that eventually wreak havoc in the brains of Alzheimer’s patients.

One of the major, relatively recent Alzheimer's discoveries is how the proteins that accumulate in tangled clusters in patients’ brains get that way. It’s largely a folding problem. The proteins abnormally fold in on themselves over and over, destroying neuron structure and connectivity as the resulting amyloid mass builds into disruptive, suffocating clumps. Most treatments to date have attempted to directly reduce amyloid protein buildup, but the latest study started with a different question: what if the folding process itself could be interrupted and reversed?

Enter the enzyme known as cyclophilin 40 (CyP40). It’s at once part of the protein disruption that causes the disease, but also the prime candidate to be harnessed and reengineered to unravel the proteins. Normally it serves as a directional guide for proteins as they bend and fold. When that process goes wrong, as it does in Alzheimer’s, the enzyme is part of the problem. But if made to work in reverse, it could undo the folding-gone-awry, or possibly prevent it from happening.

In a mouse model, researchers from the University of South Florida did essentially that and found that CyP40 reduced the buildup of amyloid tau proteins by unraveling them. Once that was accomplished, the proteins became soluble and could be more easily removed via the brain’s immune response. That reduced the degeneration of neurons, leading to fewer symptoms of the disease (specifically, the researchers say they were able to "preserve cognition" in the mice brains). The enzyme also unraveled alpha-synuclein, the protein aggregate linked to the development of Parkinson's disease. 

It’s still not entirely clear how CyP40 works (the researchers offer a couple of possibilities in the study), but this is the first time that a study has shown in an animal model that it does work as a protein unraveler. Previous lab studies showed only that it was theoretically possible to harness the enzyme’s power in an actual brain. Now we know it can be done, and that’s exciting.

Just as encouraging, CyP40 is not the only enzyme that could potentially be harnessed to work against neurodegenerative diseases. The researchers say there are in the neighborhood of 40 other enzymes that may serve a similar purpose.

Story Source: The above story is based on materials provided by FORBES

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