Intestinal Permeability, Dysbiosis, Inflammation and Enteric Glia Cells: The Intestinal Etiology of Parkinson’s Disease

Abstract

The scientific and medical communities are becoming more aware of the substantial relationship between the function of the central nervous system (CNS) and the state of the gut environment. Parkinson's disease (PD) is a neurodegenerative disorder that affects the nigrostriatal pathway in the midbrain, presenting not only motor symptoms but also various non-motor manifestations, including neuropsychiatric symptoms and gastrointestinal (GI) symptoms. Over time, our knowledge of PD has progressed from the detection of midbrain dopaminergic deficits to the identification of a multifaceted disease with a variety of central and peripheral manifestations, with increased attention to the intestinal tract. Accumulating evidence has revealed that intestinal disorders are not only the peripheral consequence of PD pathogenesis, but also the possible pathological initiator decades before it progresses to the CNS. Here, we summarized recent research findings on the involvement of the intestinal environment in PD, with an emphasis on the involvement of the intestinal barrier, microbiome and its metabolites, inflammation, and enteric glial cells.