19 November 2010

A non-immune mediated sequestering of Amyloid Beta

In a paper published in 2003, "Novel Therapeutic Approach for the Treatment of Alzheimer's Disease by Peripheral Administration of Agents with an Affinity to B-Amyloid", it was reported that in a mouse model of Alzheimer's, amyloid sequestering proteins were effective in removing CNS plaques without inducing inflammation.
In brief, the researchers utilized the idea of a CNS:Periphery dynamic system in which a shift in equilibrium could result in removal of an offending agent. To accomplish this, mice with advancing plaque formation were treated with two bovine derived factors with known ability to sequester amyloid. Mice were treated with one or the other, a third group was treated with vehicle solution.
The results showed that the treatment was effective in removing the plaques, although it was unclear whether the damage could be undone. Although this presents an interesting target for future therapy, the use in humans will depend on the mouse model being an accurate depiction of Alzheimer's pathogenesis. It was also mentioned that the treatment was most likely most effective as a prophylactic treatment, rather than a rescue treatment.

1 comment:

  1. Wow, that sounds interesting. I'm very surprised that no inflammation was induced. Where did the aggregates of the beta amyloid and bovine proteins go? Seems like phagocytes would be interested in something like that.

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