Theoretical Relevance of the Gut–Brain Axis and Black Yeast βGlucan in Parkinson’s Disease:

A Narrative Review Integrating Immunity, the Intestinal Barrier, and αSynuclein Pathology.

Abstract

Summary
In Parkinson’s disease (PD), gastrointestinal symptoms such as constipation
often precede motor symptoms by years. A “gut–brain axis” model—in which gut
dysbiosis, intestinal barrier disruption, mucosal immune activation, systemic
circulation of inflammatory cytokines, vagal pathways, and the misfolding and guttobrain
propagation of endogenous αsynuclein
(αsyn)
interact—has gained strong
support. This narrative review positions β1,3/1,6glucan
derived from the black yeast
Aureobasidium pullulans within this framework, without asserting clinical efficacy.
We organize its theoretical relevance along four axes arranged in upstreamtodownstream
causal order: (1) gut microbiota reconstitution, (2) intestinal barrier
protection, (3) recalibration of innate “trained” immunity via Dectin1
signaling, and
(4) support for the clearance of αsyn
aggregates. We further map potential effects
across five symptom domains—inflammation/immunity, constipation/gut
environment, sleep, mood/motivation, and motor symptoms. A. pullulansderived
βglucan
is emphasized because it is secreted extracellularly through fermentation as a
watersoluble
β1,3/1,6glucan,
requiring no cellwall
disruption or extraction, unlike
βglucans
from Saccharomyces cerevisiae or Aspergillus oryzae. We stress that this
review does not negate the established intracerebral pathology (nigral dopaminergic
degeneration) or dopaminereplacement
therapy; rather, it addresses the upstream,
gutderived
contribution acting in parallel. Although not established as a diseasemodifying
agent, black yeast βglucan
may reduce gutderived
inflammatory signaling
and intervene at multiple nodes of the PD gut–brain axis as an adjunctive candidate