Read with caution!

This post was written during early stages of trying to understand a complex scientific problem, and we didn't get everything right. The original author no longer endorses the content of this post. It is being left online for historical reasons, but read at your own risk.

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: