Acta Neuropathologica

, Volume 124, Issue 5, pp 665–680

Parkinson’s disease is not associated with gastrointestinal myenteric ganglion neuron loss

Authors

  • Dana M. Annerino
    • Department of Neurology and the Center for Neurodegenerative DiseaseEmory University School of Medicine
  • Shawn Arshad
    • Department of Neurology and the Center for Neurodegenerative DiseaseEmory University School of Medicine
  • Georgia M. Taylor
    • Department of Neurology and the Center for Neurodegenerative DiseaseEmory University School of Medicine
  • Charles H. Adler
    • Department of NeurologyMayo Clinic
  • Thomas G. Beach
    • Civin Laboratory of NeuropathologyBanner Sun Health Research Institute
    • Department of Neurology and the Center for Neurodegenerative DiseaseEmory University School of Medicine
Original Paper

DOI: 10.1007/s00401-012-1040-2

Cite this article as:
Annerino, D.M., Arshad, S., Taylor, G.M. et al. Acta Neuropathol (2012) 124: 665. doi:10.1007/s00401-012-1040-2

Abstract

Gastrointestinal dysfunction is a prominent non-motor feature of Parkinson’s disease (PD) that contributes directly to the morbidity of patients, complicates management of motor symptoms, and may herald incipient PD in patients without motor disability. Although PD has traditionally been considered a disease of dopaminergic neurons in the substantia nigra, analyses of gastrointestinal samples from PD patients have consistently revealed pathology in the enteric nervous system. The relationship of PD pathology to GI dysmotility is poorly understood, and this lack of understanding has led to limited success in developing treatments for PD-related GI symptoms. We have quantitatively compared myenteric neuron density and relative abundance of NO, VIP, and catecholamine neurons between patients with PD and control individuals along the length of the GI tract. In addition, we have examined the frequency of GI α-synuclein neuritic pathology and its co-localization with the same neuronal markers. We have included a comparison with a small population of patients with incidental Lewy bodies found at autopsy. These data indicate that there is no neuronal loss in the myenteric plexus in PD. Lewy body pathology parallels parasympathetic autonomic input from the dorsal motor nucleus of the vagus, not the distribution of extrinsic sympathetic input or intrinsic enteric neurons, and is only rarely co-localized with tyrosine hydroxylase. These data provide a critical background to which further analyses of the effect of PD on the GI tract may be compared and suggest that neuropathology in myenteric neurons is unlikely to be a causative factor in PD-related GI dysmotility.

Keywords

Enteric Gastrointestinal Nitric oxide Vasoactive intestinal peptide Catecholamine Acetylcholine Constipation Gastroparesis Lewy body Synuclein

Copyright information

© Springer-Verlag 2012