Prion-like proteins drive several diseases of aging, say leading neurology researchers

September 9, 2013

Prion-like protein aggregates drive the progression of several neurodegenerative diseases. a. Amyloid-beta plaques in Alzheimers. b. Neurofibrillary tangles (tau) in Alzheimer’s. c. Lewy bodies (alpha-synuclein) in Parkinson’s. d. TDP-43 inclusions in motor neurons in ALS. (Credit: Emory University/Nature)

Many of the brain diseases associated with aging, such as Alzheimer’s and Parkinson’s, are caused by specific proteins that misfold and aggregate into harmful seeds — similar to what happens with prions.

That’s a new hypothesis that two leading neurology researchers — Mathias Jucker and Lary Walker — haveproposed.

These seeds behave very much like the pathogenic agents known as prions, which cause mad cow disease, chronic wasting disease in deer, scrapie in sheep, and Creutzfeldt-Jakob disease in humans, the researchers say.

The hypothesis could unify scientists’ thinking about several neurodegenerative diseases and suggest therapeutic strategies to combat them.

Walker is research professor at Yerkes National Primate Research Center, Emory University. Jucker is head of the Department of Cellular Neurology at the Hertie Institute for Clinical Brain Research at the University of Tübingen and the German Center for Neurodegenerative Diseases./.../