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Celiac.com 12/02/2019 - Parkinson’s development can take many paths, with factors like genetics, aging, and environmental conditions all playing roles. Most people with Parkinson’s disease experience non-motor-symptoms, such as chronic constipation and/or impairment of gastrointestinal (GI) transit, long before the disease manifests clearly. Researcher Tomasza Brudek recently reviewed available medical literature for a possible link between Inflammatory Bowel Disease (IBD) and Parkinson's Disease. Brudek is affiliated with both the Research Laboratory for Stereology and Neuroscience, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital in Copenhagen, Denmark; and the Copenhagen Center for Translational Research, Copenhagen University Hospital, Bispebjerg and Frederiksberg Hospital in Copenhagen, Denmark. Build-up of α-synuclein protein in the form of Lewy bodies and Lewy neurites, and degeneration of substantia nigra dopamine neurons are classic clinical markers of Parkinson's Disease. Major features of Parkinson's Disease include inflammatory responses manifested by glial reactions, T cell infiltration, and increased expression of inflammatory cytokines, along with other toxic mediators derived from activated glial cells. Experimental, clinical and epidemiological data suggest that intestinal inflammation influences the development of Parkinson's Disease, while more and more studies suggest that Parkinson's disease may begin in the gut long before any motor symptoms show up. Patients with inflammatory bowel disease (IBD) have a higher risk of developing Parkinson's Disease compared with non-IBD individuals. Gene association study has found a genetic link between IBD and Parkinson's Disease, and an evidence from animal studies suggests that gut inflammation, similar to that observed in IBD, may induce loss of dopaminergic neurons. Based on preclinical models of Parkinson's Disease, some clinicians hypothesize that the early stages of early in Parkinson's Disease are marked by enteric microbiome changes, and gut infections triggering α-synuclein release and aggregation. Because gastrointestinal pathology can play such an important role in Parkinson's Disease development, there's good reason to believe that IBD and IBD treatments can influence Parkinson's Disease risk. This review underscores how important it is for physicians to be aware of Parkinson's Disease symptoms in IBD patients. Read more in the Journal of Parkinson's Disease, vol. 9, no. s2, pp. S331-S344, 2019
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Celiac.com 05/16/2018 - Galectins are a family of animal lectins marked by their affinity for N-acetyllactosamine-enriched glycoconjugates. Galectins control several immune cell processes and influence both innate and adaptive immune responses. A team of researchers recently set out to assess the role of galectins, particularly galectin-1 (Gal-1), in the treatment of celiac disease. The research team included Victoria Sundblad, Amado A. Quintar, Luciano G. Morosi, Sonia I. Niveloni, Ana Cabanne, Edgardo Smecuol, Eduardo Mauriño, Karina V. Mariño, Julio C. Bai, Cristina A. Maldonado, and Gabriel A. Rabinovich. The researchers examined the role of galectins in intestinal inflammation, particularly in Crohn’s disease, ulcerative colitis, and celiac disease patients, as well as in murine models resembling these inflammatory conditions. Maintaining the fine balance between host immunity and tolerance promotes gut homeostasis, and helps to prevent inflammation. To gain insight into the role of Gal-1 in celiac patients, the team demonstrated an increase in Gal-1 expression following a gluten-free diet along with an increase in the frequency of Foxp3+ cells. The resolution of the inflammatory response may promote the recovery process, leading to a reversal of gut damage and a regeneration of villi. Among other things, the team’s findings support the use of Gal-1 agonists to treat severe mucosal inflammation. In addition, Gal-1 may serve as a potential biomarker to follow the progression of celiac disease treatment. Gut inflammation may be governed by a coordinated network of galectins and their glycosylated ligands, triggering either anti-inflammatory or pro-inflammatory responses. That network may influence the interplay between intestinal epithelial cells and the highly specialized gut immune system in physiologic and pathologic settings. The team’s results demonstrate that the anti-inflammatory and tolerogenic response associated with gluten-free diet in celiac patients is matched by a substantial up-regulation of Gal-1. This suggests a major role of this lectin in favoring resolution of inflammation and restoration of mucosal homeostasis. This data highlights the regulated expression of galectin-1 (Gal-1), a proto-type member of the galectin family, during intestinal inflammation in untreated and treated celiac patients. Further study of this area could lead to better understanding of the mechanisms behind celiac disease, and potentially to a treatment of the disease. Source: Front. Immunol., 01 March 2018. The researchers in this study are variously affiliated with the Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina; the Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Córdoba, Argentina; the Laboratorio de Glicómica Funcional y Molecular, Instituto de Biología y Medicina Experimental (IBYME), Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Sección Intestino Delgado, Departamento de Medicina, Hospital de Gastroenterología Dr. C. Bonorino Udaondo, Buenos Aires, Argentina; the Unidad de Patología, Hospital de Gastroenterología, Bonorino Udaondo, Buenos Aires, Argentina; the Instituto de Investigaciones, Universidad del Salvador, Buenos Aires, Argentina; and the Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.