Currently, there is a gap in the knowledge of the factors that govern the infectious potential of amyloid in general. In an article published in the journal eLife, Dr Xue's team report on their investigations into why some forms of amyloid are highly infectious - the so-called prion form associated with BSE (Mad Cow Disease) and the human form, CJD (Creutzfeldt Jakob Disease) - while others are less infectious or even inert.
They discovered that the infectious potential of an amyloid is a complex biological property better described on a sliding scale rather than either one category (transmissible prions) or another (non-transmissible amyloid), as it is now.
Currently most amyloids apart from prions are viewed as non-transmissible between individuals meaning people would be unable to 'catch' Alzheimer's or Parkinson's simply by association. This research sheds new light on why some amyloid forms can potentially spread between cells and tissues within the same individual, and some are considered prions that are transmissible from one individual to another.
Ricardo Marchante, David M Beal, Nadejda Koloteva-Levine, Tracey J Purton, Mick F Tuite, Wei-Feng Xue.
The physical dimensions of amyloid aggregates control their infective potential as prion particles.
eLife 2017;6:e27109 doi: 10.7554/eLife.27109.