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: