Gastrointestinal dysmotility in rodent models of Parkinson's disease

Am J Physiol Gastrointest Liver Physiol. 2024 Jan 23. doi: 10.1152/ajpgi.00225.2023. Online ahead of print.ABSTRACTMultiple studies describe prodromal, non-motor dysfunctions that affect the quality of life of patients who subsequently develop Parkinson's disease (PD). These prodromal dysfunctions comprise a wide array of autonomic issues, including severe gastrointestinal (GI) motility disorders such as dysphagia, delayed gastric emptying and chronic constipation. Indeed, strong evidence from studies in humans and in animal models suggests that the GI tract and its neural, mainly vagal, connection to the central nervous system (CNS) could have a major role in the aetiology of PD. In fact, misfolded α-synuclein aggregates that form Lewy bodies and neurites, i.e. the histological hallmarks of PD, are detected in the enteric nervous system (ENS) prior to clinical diagnosis of PD. The aim of the present review is to provide novel insights on the pathogenesis of GI dysmotility in PD, focusing our attention on functional, neurochemical and molecular alterations in animal models.PMID:38261717 | DOI:10.1152/ajpgi.00225.2023
Source: Am J Physiol Gastroi... - Category: Gastroenterology Authors: Source Type: research