Vagal motoneurons in Parkinson’s disease

Ruth E. Musgrove, Wei Hua Chiu, Joshua A. Goldberg

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

1 Scopus citations

Abstract

The dorsal motor nucleus of the vagus nerve (DMV) is among the first regions affected by Lewy pathology in Parkinson’s disease (PD). Neuropathology in the DMV is thought to contribute to the prodromal non-motor manifestations of disease, such as a decline in gastrointestinal motility. Because vagal motoneurons are affected so early in PD, considerable efforts have focused on understanding their role in the pathogenic and progressive mechanisms of the disease. Two distinct theories that explain the origin of DMV pathology have been proposed. The first states that cell-autonomous characteristics determine neuronal susceptibility to environmental, genetic, or age-related disease contributors. The second prion-like hypothesis attributes the pathogenesis and progression of disease to processes of protein misfolding, seeding, and perpetual self-replication. These aberrant protein species are thought to propagate pathology by cell-to-cell transfer through neuronal networks. We will discuss experimental evidence for the involvement of the DMV in each of these hypotheses. We propose that a consideration of cell-autonomous factors could be useful to explain how prion-like protein pathology progresses through complex neuronal networks to affect only certain predisposed neuronal populations.

Original languageAmerican English
Title of host publicationGenetics, Neurology, Behavior, and Diet in Parkinson’s Disease
Subtitle of host publicationThe Neuroscience of Parkinson’s Disease, Volume 2
PublisherElsevier
Pages327-343
Number of pages17
ISBN (Electronic)9780128159507
DOIs
StatePublished - 1 Jan 2020

Bibliographical note

Publisher Copyright:
© 2020 Elsevier Inc.

Keywords

  • DMV
  • Dorsal motor nucleus of the vagus nerve
  • Gastrointestinal dysfunction
  • Gut-brain axis
  • Lewy pathology
  • Neuron-to-neuron protein spreading
  • Prion-like hypothesis
  • Selective vulnerability
  • α-Synuclein

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