A bioactive capsule packed with antibody producing cells could reduce amyloid build up in Alzheimer’s
Alzheimer’s is a complex disease we still don’t fully understand, but it’s apparent amyloid plaques play some role in the condition – interfering with brain function. Previous attempts to deliver antibodies to these amyloid clumps in order to stimulate immune clearance have proved largely ineffective, as large doses can cause a number of complications. The solution is therefore to deliver a slow, small stream of antibodies that prevent the toxic build up seen in Alzheimer’s patients.
A new implant
In a new proof of concept experiment, researchers from Switzerland have now tested a small capsule filled with cells genetically engineered to produce anti-amyloid antibodies; designed to be placed just under the skin. In mice these implants were able to produce antibodies for 10 months and importantly reduce amyloid accumulation.
How did they do it?
Building on previous work, mouse cells were infected with a modified virus carrying the antibody gene – Mab-11. Because implanting these cells outright would trigger an immune response, they encapsulated them in a porous material that would allow antibodies to leak out and nutrients to enter. The cells were injected into a chamber inside filled with hydrogel.
The capsule was tested on two mice models of Alzheimer’s disease, with mutations that mirror those seen in people with familial Alzheimer’s. They found that not only were the cells healthy after 9 months implantation, but Mab-11 antibodies were successfully tagging amyloid in the brain. This triggered the brain’s immune cells Microglia to gobble them up.
When they tested the implant on mice who had yet to develop the characteristic plaques, they discovered it was able to inhibit plaque accumulation by up to 95%
Not a perfect solution
While this is certainly an innovative, intriguing approach, unfortunately some mice seemed to develop a tolerance and mounted an immune response to these Mab-11 antibodies. This can be blocked with immunosuppressants, but that’s hardly ideal long term. It may be that antibodies would have to be changed every few months in order to remain effective.
An additional question is whether stopping amyloid in itself will have a therapeutic effect, as there are many other facets to Alzheimer’s that we don’t fully understand. It could be that we’ll have to fix multiple problems before any real protection is seen. It’s still a great new concept however that could be applied to many more diseases in the future.
Check out a cartoon from the École polytechnique fédérale de Lausanne (EPFL) about the approach below:
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