Curing Alzheimer’s Disease With Potent Brain Molecule
Curing Alzheimer’s: Introducing VPS35, Brain Molecule
Research scientists at Temple University in Philadelphia, PA, showed that they could control tau buildup by altering levels of VPS35.
VPS35 sorts out and transports the dysfunctional proteins to degradation sites. In addition, the effectiveness of VPS35 against tau proteins, also depends on an enzyme called cathepsin D, which is a catalyst that helps break down proteins in the cells.
Curing Alzheimer’s: VPS35 and Tau
The correct folding of proteins is necessary for cell functioning. If they fold incorrectly, they do not perform properly and can disrupt vital processes. To protect against this, cells have mechanisms for clearing out defective proteins.
Nevertheless, the buildup of faulty proteins does occur. Neurons are particularly vulnerable to misfolded protein deposits because of their unique biology. This vulnerability could explain why defective protein accumulation often is found in neuro-degenerative diseases.
Tau is one of the most common proteins to form toxic deposits in the brain. Scientists call this condition tauopathy.
And, in addition, previous studies reported that people with Alzheimer’s disease have below normal levels of VPS35 in their brains.
For their study, the team used brain tissue from people with Picks’ disease. Their toxic protein deposits only come from defective tau.
The researchers found that levels of VPS35 were 50% lower in the Picks’ samples than in brain tissue of people who did not have a neuro-degenerative disease.
In experiments on cultured human cells, they found that they could directly control the amount of tau buildup by altering levels of VPS35.
This is the first study to show that VPS35 has a role in tauopathy.
Next, the team altered VPS35 levels in mice with tau buildup in their brains. They showed that reducing VPS35 worsened the animals’ memory and learning abilities and impaired movement control.
When the researchers examined the animals’ brain tissues, they found that lowering VPS35 had disrupted synapses in neurons and considerably damaged their ability to communicate.
The animals lost about 40–50% of their synaptic connectivity as a result of lowering VPS35.
Curing Alzheimer’s: Conclusion
The research team suggests it could be possible to develop a drug that restores VPS35 function in neuro-degenerative diseases, such as Alzheimer’s. They are already planning to investigate this possibility.