Publications by authors named "C Segnani"
Correction for ' HEAL9 attenuates cognitive impairment and progression of Alzheimer's disease and related bowel symptoms in SAMP8 mice by modulating microbiota-gut-inflammasome-brain axis' by C. Di Salvo , , 2024, , 10323-10338, https://doi.org/10.
View Article and Find Full Text PDF: Growing evidence highlights the relevance of the microbiota-gut-brain axis in Alzheimer's disease (AD). AD patients display gut dysbiosis, altered intestinal barrier and enteric inflammation that, besides bowel symptoms, can contribute to brain pathology. In this context, the modulation of gut microbiota is emerging as a therapeutical option to halt or slow down central pathology.
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- This study explores how the NLRP3 inflammasome influences changes in the intestinal epithelial barrier (IEB) linked to obesity, particularly focusing on interactions between enteric glia and intestinal epithelial cells (IECs).
- Mice on a high-fat diet exhibited weight gain, compromised IEB integrity, increased glial cells, and NLRP3 inflammasome activation; however, NLRP3-deficient mice had less weight gain and better IEB integrity.
- The findings suggest that the NLRP3 inflammasome in enteric glia could be a potential target for new drugs to improve IEB integrity in obesity-related conditions.
Background: Elevated levels of prokineticin-2 (PK2), regarded as a protein involved in modulating immune/inflammatory responses, have been detected in the substantia nigra, serum, and olfactory neurons of Parkinson's disease (PD) patients. Of note, emerging evidence suggests that gut alterations, including dysbiosis and enteric inflammation, play a role in PD via the gut-brain axis.
Objectives: Our goal was to investigate the expression of PK2 in colonic biopsies of PD patients.
Intestinal barrier alterations represent a primum movens in obesity and related intestinal dysfunctions. However, whether gut barrier remodeling represents prodromal events in obesity before weight gain, metabolic alterations, and systemic inflammation remains unclear. Herein, we examined morphologic changes in the gut barrier in a mouse model of high-fat diet (HFD) since the earliest phases of diet assumption.
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