A new study published in Science describes the success of a cancer drug in clearing beta-amyloid plaques in murine models.

The job of removing beta-amyloid is performed by the enzyme apolipoprotein E (ApoE).  In people with a variant of this enzyme, beta-amyloid may stop being removed effectively.  People with the ApoE4 variant in paritcular are at higher risk of this happening and consequently developing Alzheimer’s disease.

A few questions:

  • Can this drug work for misfolded PrP plaques?
  • Is there an enzyme that clears away PrP equivalently?
  • If such an enzyme exists, when and why does it clear PrP away?  Does it normally clear misfolded PrP away only?  Does PrP misfold on occasion normally?
  • If such an enzyme exists, can a variant in the enzyme make a patient immune to misfolded PrP?  Could some people, such as kuru survivors, have such a variant?

Studying the role and lifecycle of PrP is a good funding target.  What information is out there already?

Along these lines of thinking, it would be great if we could get access to a genomic database and start looking for variations in PrP among the population, variations in the genomes of kuru survivors, and variations in the genome of people at the PrP-clearing enzyme (if it exists).

Links the work:

http://www.sciencemag.org/content/early/2012/02/08/science.1217697

http://www.bbc.co.uk/news/health-16945466