alexa Neuronal Protein Alteration in Enteric Dysmotility Syndrome | OMICS International | Abstract
ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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Short Communication

Neuronal Protein Alteration in Enteric Dysmotility Syndrome

Irina Alafuzoff1,2*, Svetlana N. Popova2, Alkwin Wanders3 and Bela Veress4

1Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden

2Department of Clinical Pathology, Uppsala University Hospital, Uppsala, Sweden

3Department of Clinical Pathology and Cytology, Umea University Hospital, Umea, Sweden

4Department of Clinical Pathology and Cytology, Skane University Hospital, Malmo, Sweden

Corresponding Author:
Irina Alafuzoff
Department of Immunology, Genetics and Pathology
Uppsala University Hospital, Rudbeck Laboratory
Dag Hammarskjölds väg 20, 751 85, Uppsala, Sweden
Tel: +46 (0) 706114822
E-mail: [email protected]

Received date: January 08, 2016; Accepted date: February 10, 2016; Published date: February 16, 2016

Citation: Alafuzoff I, Popova SN, Wanders A, Veress B (2016) Neuronal Protein Alteration in Enteric Dysmotility Syndrome. J Alzheimers Dis Parkinsonism 6:212. doi:10.4172/2161-0460.1000212

Copyright: © 2016 Alafuzoff I, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Little is known about the enteric ganglionic system in subjects with gastrointestinal dysmotility syndrome (GIDS). Furthermore, dysfunction of gastrointestinal motility is an early complaint of subjects with Parkinson’s disease.

Here, we assessed p62/sequestosome-1(p62) and α-synuclein (αS) immunoreactivity (IR) in full-thickness bowel specimens of the gut obtained from six subjects with GIDS and from 17 controls.

In the myenteric neurons, fine punctuate p62-IR were seen in all of the controls, whereas diffuse cytoplasmic and nuclear p62-IR were seen in the GIDS cases. Physiological αS-IR (clone 42/αS) was seen in all of the controls and the GIDS cases in the lamina propria, the submucosal and in the myenteric plexuses. The disease associated αS (clone 5G4) labeled the cytoplasm of the ganglion cells only in the myenteric plexus in three out of the four subjects with the GIDS/inflammatory neuropathy.

In summary, ganglion cells were readily visualized in all of the layers of the bowel with clone 42/αS, and p62 displayed altered patterns of labeling in subjects with the GIDS. Labeling seen with the disease associated clone 5G4/αS in the GIDS/inflammatory neuropathy is intriguing and might indicate that the alteration of αS is triggered by a chronic inflammation.


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