Scientific American – May-June 2019, Volume 30, Number 3

THE ARTFUL AMOEBA

The Case for

Transmissible

Alzheimer’s

Grows

What separates a lethal prion from

a dementia-associated amyloid plaque?

Maybe not much

T

he unsettling evidence that Alzheimer’s dis-

ease may be transmissible under limited—

but definitely nonzero—circumstances

keeps growing.

Last December I wrote about research that re-

vealed that infectious, lethal proteins called prions

have the potential to be transmitted on optical

medical equipment because they are present

throughout the eyes of victims.

This was all the more disturbing in light of a

study I had also recently written about that sug-

gested that peptide aggregates—essentially sticky,

self-propagating clumps of misfolded protein bits

collectively referred to as amyloid—found in the

brains of Alzheimer’s patients may be transmissible

in the same ways that prions are.

Then, just a few days after I wrote about the

prion eye hazard, a new paper appeared inNature

that seemed to take the evidence for the transmis-

sibility of Alzheimer’s peptides from “circumstantial”

to “experimentally produced.” It is fascinating, if un-

settling, news, that further blurs the line between

amyloid and prions.

Human prion diseases are rare. Prions usually

form spontaneously or are inherited via faulty JUAN GAERTNER

GETTY IMAGES

Jennifer Frazer is an AAAS Science Journalism Award-

winning science writer. She has degrees in biology,

plant pathology/mycology and science writing, and has

spent many happy hours studying life in situ.

Opinion

Orange amyloid beta plaques

accumulate on a neuron in this

computer-generated image

illustrating the pathology of

Alzheimer’s disease.