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A New Alzheimer’s Model: It Takes Two

Posted on 5 July 2016

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Credit: Spike Walker, Wellcome Images  

Credit: Spike Walker, Wellcome Images  

A new mouse model has revealed that beta amyloid plaques are likely insufficient to cause Alzheimer’s by themselves – it takes formation of a protein called tau too in a complex interplay

There are two main culprits when it comes to Alzheimer’s: tau and beta amyloid. While there have been a great many developments in recent years, it’s still unclear exactly what processes trigger disease onset. There is now some evidence that beta amyloid accumulation might be a dysfunctional response to infection, but there are still many conflicting theories about which processes actually lead to brain damage. 

A toxic combination

We know that beta amyloid clumps are commonly found in Alzheimer’s brains outside of neurons, and tangles of a protein called tau are found inside them. But which comes first, and are they connected? 

Now, new research at John Hopkins University is suggesting that beta amyloid accumulation in itself (regardless of the reason for its accumulation), isn’t enough to cause tau conversion. The latest work hints that beta amyloid sets off a complex chain of chemical events that eventually lead to formation of tau tangles – 10-15 years after accumulation. This could partly explain why beta amyloid plaques are frequently found in patients without any Alzheimer’s symptoms, as there are clearly complicated other influencing factors. 

“For the first time, we think we understand that the accumulation of amyloid plaque alone can damage the brain, but that’s actually not sufficient to drive the loss of nerve cells or behavioral and cognitive changes. What appears to be needed is a second insult—the conversion of tau—as well.”

A new mouse model

In humans with Alzheimer’s disease, in in Parkinson’s patients, the actual disease process begins many years before symptom onset. If beta amyloid really does set off a chain of events that lead to tau tangles over 10 years later, then mice are an extremely poor disease model – having only a 2-3 year life span. To address this issue, the John Hopkins team genetically engineered a new mouse strain to produce a tau fragment associated with clumping. This fragment alone wasn’t sufficient to create tau tangles, but crucially when neurons were exposed to beta amyloid plaques, tau accumulation began. 

It takes two

What’s more, the research suggests that it indeed takes both tau and beta amyloid to trigger real neuron damage, but that it is the conversion of tau that really speeds up destruction. If we could find a way to interfere with this gradual conversion process then we may be able to halt disease onset. 

“If you were to intervene in the time period before the conversion of tau, you might have a good chance of ameliorating the deficits, brain cell loss and ensuing consequence of the disease”

Read more at NeuroscienceNews

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