Testing the Protein Propagation Hypothesis of Parkinson Disease

Journal of Experimental Neuroscience
Alain Dagher, Yashar Zeighami

Abstract

One of the most exciting recent hypotheses in neurology is that most neurodegenerative diseases are caused by the neuron to neuron propagation of prion-like misfolded proteins. In Parkinson disease, the theory initially emerged from postmortem studies demonstrating a caudal-rostral progression of pathology from lower brainstem to neocortex. Later, animal studies showed that the hallmark protein of PD, α-synuclein, exhibited all the characteristics of a prion. Here, we describe our work using human neuroimaging to test the theory that PD pathology advances via a propagating process along the connectome. We found that the pattern and progression of brain atrophy follow neuronal connectivity, correlate with clinical features, and identify an epicenter in the brainstem.

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Citations

Mar 3, 2020·Critical Reviews in Clinical Laboratory Sciences·Darren M O'HaraLorraine V Kalia
Aug 20, 2019·Neurotoxicity Research·Brian Hansen
May 10, 2019·Frontiers in Neuroscience·Emily FitzgeraldHolly A Martinson
Jul 18, 2020·Nature Communications·Monja P NeuserNils B Kroemer
Sep 13, 2019·NeuroImage. Clinical·Yashar ZeighamiAlain Dagher

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