Published on: July 11, 2019
by Medical Daily:
Alzheimer’s is one of the most common neurodegenerative diseases affecting millions today. Usually targeting people aged 60 and above, it works by slowly killing the neurons in various parts of our brain, making the person suffering from it start to slowly lose “themselves,” oftentimes making them forgetful and damaging their memory.
One prominent feature in its development is the buildup of defective tau proteins, which gets tangled with our nerve cells and neurons, killing them and disrupting brain function.
Now, scientists may have just identified a molecule that can help prevent its buildup in the first place, marking another step to finally curing the devastating disease.
Published in a Molecular Pyschiatry study paper, the scientists were able to identify a molecule with the name vacoular protein sorting 35 (VP35) that picks apart faulty tau proteins and removes them from the system.
“A major part of what VPS35 does is to sort out and transport dysfunctional proteins to degradation sites,” said senior study author Prof. Domenico Praticò, director of LKSOM’s Alzheimer’s Center at Temple.
To do this, Praticò and his team used human cells to show that they can control the buildup of tau via altering the levels of VP35. Besides this, they also discovered the protein’s effect on tau also depends on cathepsin D activity, which is an enzyme that breaks down the protein in cells.
In their study, the team made use of brain tissue from people suffering from either Progressive Supra-nuclear Palsy (PSP) or Picks’ disease. The choice was made given these two conditions are also connected to defective tau.
According to previous studies, problems with VP35 is related to Alzheimer’s disease, with results showing that people with less VP35 are more likely to develop the condition later on.
However, before Praticò’s research, it was unclear how the two are connected.
Moving forward, the team plans to develop a drug that could help restore proper VP35 function in people suffering from neurodegenerative diseases, and are now planning to further investigate the possibility. The team also plans on finding another way to approach the mechanisms that cause tau buildup in the first place.
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