Microbiota-gut-brain signalling in Parkinson's disease: Implications for non-motor symptoms

Valeria D. Felice, Eamonn Martin Quigley, Aideen M. Sullivan, Gerard W. O'Keeffe, Siobhain M. O'Mahony

Research output: Contribution to journalArticle

88 Scopus citations

Abstract

Parkinson's disease is the second most common neurodegenerative disorder, affecting 1-2% of the population over 65 years of age. The primary neuropathology is the loss of midbrain dopaminergic neurons, resulting in characteristic motor deficits, upon which the clinical diagnosis is based. However, a number of significant non-motor symptoms (NMS) are also evident that appear to have a greater impact on the quality of life of these patients.In recent years, it has become increasingly apparent that neurobiological processes can be modified by the bi-directional communication that occurs along the brain-gut axis. The microbiota plays a key role in this communication throughout different routes in both physiological and pathological conditions. Thus, there has been an increasing interest in investigating how microbiota changes within the gastrointestinal tract may be implicated in health and disease including PD.Interestingly α-synuclein-aggregates, the cardinal neuropathological feature in PD, are present in both the submucosal and myenteric plexuses of the enteric nervous system, prior to their appearance in the brain, indicating a possible gut to brain route of "prion-like" spread. In this review we highlight the potential importance of gut to brain signalling in PD with particular focus on the role of the microbiota as major player in this communication.

Original languageEnglish (US)
JournalParkinsonism and Related Disorders
DOIs
StateAccepted/In press - Nov 5 2015

Keywords

  • Brain-gut axis
  • Depression
  • Microbiota
  • Pain
  • Parkinsons disease

ASJC Scopus subject areas

  • Geriatrics and Gerontology
  • Clinical Neurology
  • Neurology

Fingerprint Dive into the research topics of 'Microbiota-gut-brain signalling in Parkinson's disease: Implications for non-motor symptoms'. Together they form a unique fingerprint.

Cite this