Percorrer por autor "Carregosa, Ricardo"
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- Gut status in Parkinson’s disease: the GutSPark protocolPublication . Grunho, Miguel; Godinho, Catarina; Matos, António Alves de; Barroso, Helena; Carregosa, Ricardo; Marx, Frederico; Tomé, Morgane; Domingos, Josefa; Sousa-catita, Diogo; Botelho, João; Machado, Vanessa; Mendes, José João; Outeiro, Tiago; Fonseca, JorgeThe neuropathological hallmark of Parkinson’s disease (PD) is the accumulation of alpha–synuclein (AS) aggregates. The identification of AS aggregates in gut biopsy specimens from people with PD may provide an opportunity to identify PD at a very early stage, prior to symptom onset. Changes in gut microbiota and inflammatory conditions (such as periodontitis) may be linked with PD onset/evolution. This project aims to explore the concept of microbiota–gut–brain axis in PD, studying gut biopsy specimens for AS aggregates, oral and intestinal microbiota, associated digestive disorders and oral health, of both patients with PD and controls.
- Inflammatory bowel disease, alpha-synuclein aggregates and Parkinson’s disease: the InflamaSPark protocolPublication . Grunho, Miguel; Godinho, Catarina; Patita, Marta; Mocanu, Irina; Vieira, Ana Isabel; De Matos, António; Carregosa, Ricardo; Marx, Frederico; Tomé, Morgane; Sousa-Catita, Diogo; Proença, Luís; Outeiro, Tiago; Fonseca, JorgeThe hallmark of Parkinson’s disease (PD) is the accumulation of alpha-synuclein (AS) aggregates. Prior to the central nervous system involvement, PD establishes itself in the gut as a result of the complex interplay between microbiota, the host’s immune/neural systems and increased intestinal permeability. Inflammatory Bowel Disease (IBD) patients present a higher number of AS aggregates in the intestinal wall and an increased risk of developing PD. By studying AS aggregates in gut biopsy specimens of IBD patients and controls, this project aims to further clarify the pathophysiology of PD and to explore the potential of gut a biopsy for AS aggregates as a biomarker for prodromal PD.
- Nutritional and motor functional status in Parkinson’s disease: the NutriSPark protocolPublication . Grunho, Miguel; Godinho, Catarina; Sousa-Catita, Diogo; Vicente, Filipa; Proença, Luís; Carregosa, Ricardo; Marx, Frederico; Tomé, Morgane; Domingos, Josefa; Fonseca, JorgeA growing body of evidence suggests that nutritional status may play an important role in the development and course of Parkinson’s disease (PD). Nutritional status is known to influence PD motor and non-motor features and is in turn influenced by disease duration and severity. A proper nutritional status assessment and intervention should be incorporated in the management and follow-up of PD patients. This study aims to characterize the impact of nutritional status in multiple domains of PD and to explore the feasibility and the effectiveness of a customized and intensive nutritional intervention compared to standard care.
- Prolonged fasting induces histological and ultrastructural changes in the intestinal mucosa that may reduce absorption and revert after enteral refeedingPublication . Nunes, Gonçalo; Guimarães, Marta; Coelho, Hélder; Carregosa, Ricardo; Oliveira, Cátia; Pereira, Sofia S.; Matos, António Alves de; Fonseca, JorgeBackground: Malnutrition is usual in patients referred for endoscopic gastrostomy (PEG). Refeeding syndrome is rarely observed in PEG-fed patients, which could possibly be associated with reduced absorption induced by prolonged starvation. Objective: In patients submitted to PEG after a significant period of fasting, the present study aims to: 1. evaluate the histological/ultrastructural initial changes in the intestinal mucosa, potentially associated with reduced absorption, and 2. assess if these changes could reverse with enteral refeeding. Methods: The present study is an observational, prospective, controlled study. Adult patients with ingestion below 50% of daily needs for at least one month and/or diagnosis of malnutrition were enrolled. Duodenal biopsies were taken at baseline and after 3–6 months of PEG feeding, which then underwent histological/ultrastructural analysis. Random healthy individuals were used as controls. Results: A total of 30 patients (16 men/14 women) aged 67.1 ± 13.5 years were included. Malnutrition was found in 40% of patients. Approximately 14 patients completed follow-up during both periods (46.7%). At baseline: duodenal mucosal atrophy was evident in three patients (10%); the median villi length (MVL) was 0.4 mm (0.25–0.6 mm), with it being shorter than the controls, which was 0.6 mm (0.4–0.7 mm) (p = 0.006); ultrastructural changes included focal shortening, bending, and disruption of enterocyte microvilli, the presence of citoplasmatic autophagic vacuoles, dilation and vesiculation of the smooth endoplasmic reticulum, and the presence of dilated intercellular spaces with basement membrane detachment. After refeeding, most patients displayed normal histology (92.9%) and increase MVL (p < 0.001), ultrastructural changes disappeared, and enterocytes resumed a normal appearance, although retaining scarce, small, dense bodies in apical regions from the evolution of previous autophagy. Conclusions: Prolonged fasting induces histological and ultrastructural changes in the intestinal mucosa that may reflect impaired absorption in the early post-PEG period. These changes were reverted after refeeding with enteral nutrition.