TNBS colitis induces architectural changes and alpha-synuclein overexpression in mouse distal colon: A morphological study DOI Creative Commons
Arianna Casini, Giorgio Vivacqua, Ludovica Ceci

и другие.

Cell and Tissue Research, Год журнала: 2024, Номер unknown

Опубликована: Дек. 10, 2024

Alpha-synuclein (α-syn) is widely expressed in presynaptic neuron terminals, and its structural alterations play an important role the pathogenesis of Parkinson's disease (PD). Aggregated α-syn has been found brain, peripheral nerves enteric nervous system (ENS) intestinal neuroendocrine cells during synucleinopathies inflammatory bowel disorders. In present study, we evaluated histomorphological features murine colon with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, a common model colitis. Thereafter, investigated expression α-syn, Toll-like receptor 4 (TLR4), choline acetyltransferase (ChAT), vasoactive peptide (VIP), tyrosine hydroxylase (TH), calcitonin gene-related (CGRP), calcitonin-like (CALCR). Finally, presence phosphorylated (pS129 α-syn) aggregates their relationship cells. Colon from TNBS mice showed increase infiltrate significative changes architecture mucosa. α-Syn was significantly higher inflamed colon. VIP increased both mucosa muscularis externa mice, while TH, CGRP, CALCR were reduced mice. Amyloid pS129 detectable ENS, as macrophages around glands correlating markers inflammation. This study describes - for first time altered occurrence amyloid under supporting critical inflammation involvement IBD.

Язык: Английский

Comparison of vagus nerve cross-sectional area between brain-first and body-first Parkinson’s disease DOI Creative Commons

Shuangshuang Dong,

Bo Shen, Xu Jiang

и другие.

npj Parkinson s Disease, Год журнала: 2024, Номер 10(1)

Опубликована: Дек. 5, 2024

The vagus nerve (VN) is the main neural pathway linking gut and brain in Parkinson's disease (PD). In this study, we utilized high-resolution ultrasound to measure VN cross-sectional area (CSA) 96 healthy controls (HCs) 75 PD patients. group was further categorized into three subgroups: PD-preRBD, PD-postRBD, PD-nonRBD. PD-preRBD body-first subtype, PD-postRBD PD-nonRBD were brain-first subtype. had a significantly lower CSA than HCs. Subgroup analysis revealed that tended exhibit smaller both groups. CSA, specifically right VN, correlated with subtype some components of PD-related assessment scales. Overall, these findings provide evidence atrophy PD, especially suggesting could serve as an adjunctive diagnostic tool.

Язык: Английский

Процитировано

0
TNBS colitis induces architectural changes and alpha-synuclein overexpression in mouse distal colon: A morphological study DOI Creative Commons
Arianna Casini, Giorgio Vivacqua, Ludovica Ceci

и другие.

Cell and Tissue Research, Год журнала: 2024, Номер unknown

Опубликована: Дек. 10, 2024

Alpha-synuclein (α-syn) is widely expressed in presynaptic neuron terminals, and its structural alterations play an important role the pathogenesis of Parkinson's disease (PD). Aggregated α-syn has been found brain, peripheral nerves enteric nervous system (ENS) intestinal neuroendocrine cells during synucleinopathies inflammatory bowel disorders. In present study, we evaluated histomorphological features murine colon with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, a common model colitis. Thereafter, investigated expression α-syn, Toll-like receptor 4 (TLR4), choline acetyltransferase (ChAT), vasoactive peptide (VIP), tyrosine hydroxylase (TH), calcitonin gene-related (CGRP), calcitonin-like (CALCR). Finally, presence phosphorylated (pS129 α-syn) aggregates their relationship cells. Colon from TNBS mice showed increase infiltrate significative changes architecture mucosa. α-Syn was significantly higher inflamed colon. VIP increased both mucosa muscularis externa mice, while TH, CGRP, CALCR were reduced mice. Amyloid pS129 detectable ENS, as macrophages around glands correlating markers inflammation. This study describes - for first time altered occurrence amyloid under supporting critical inflammation involvement IBD.

Язык: Английский

Процитировано

0