CAPTCHA some cancer cells

Lee Cooper and colleagues explore crowdsourcing in pathology -- using slides from the Cancer Genome Read more

Bird flu shuffle probes viral compatibility

The good news is that packaging signals on the H5 and H7 viral RNA genomes are often incompatible with the H3N2 viruses. But mix and match still occurred at a low level, particularly with Read more

A life consumed by sleep

Nothing he tried had worked. For Sigurjon Jakobsson, the trip to Atlanta with his family was a last-ditch effort to wake up. He had struggled with sleeping excessively for several years before coming from Iceland to see a visionary neurologist, who might have answers. In high school, Sigurjon was a decathlete competing as part of Iceland’s national sports team. But at the age of 16, an increasing need for sleep began to encroach upon his life. Read more

Matthias Jucker

Do Alzheimer’s proteins share properties with prions?

If you’ve come anywhere near Alzheimer’s research, you’ve come across the “amyloid hypothesis” or “amyloid cascade hypothesis.”

This is the proposal that deposition of amyloid-beta, a major protein ingredient of the plaques that accumulate in the brains of Alzheimer’s patients, is a central event in the pathology of the disease. Lots of supporting evidence exists, but several therapies that target beta-amyloid, such as antibodies, have failed in large clinical trials.

Jucker_Walker_May_2014

Lary Walker and Matthias Jucker in Tübingen, 2014

In a recent Nature News article, Boer Deng highlights an emerging idea in the Alzheimer’s field that may partly explain why: not all forms of aggregated amyloid-beta are the same. Moreover, some “strains” of amyloid-beta may resemble spooky prions in their ability to spread within the brain, even if they can’t infect other people (important!).

Prions are the “infectious proteins” behind diseases such as bovine spongiform encephalopathy. They fold into a particular structure, aggregate and then propagate by attracting more proteins into that structure.

Lary Walker at Yerkes National Primate Research Center has been a key proponent of this provocative idea as it applies to Alzheimer’s. To conduct key experiments supporting the prion-like properties of amyloid-beta, Walker has been collaborating with Matthias Jucker in Tübingen, Germany and spent four months there on a sabbatical last year. Their paper, describing how aggregated amyloid-beta is “seeded” and spreads through the brain in mice, was recently published in Brain Pathology.
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Posted on by Quinn Eastman in Neuro Leave a comment