SCIENTIFIC HUB

Follow the evidence.

SCIENTIFIC LITERATURE · MED

Gut-to-Brain α-Synuclein Transmission in Parkinson's Disease: Evidence for Prion-like Mechanisms.

Int J Mol Sci · 2023-04-13

DOI: 10.3390/ijms24087205PMID: 37108366

Open accessreview-article; Review; Journal ArticleOriginal source ↗

Research overview

The text below is the source article’s original abstract under a verified reuse license. cc by

Parkinson's disease (PD) is a multifactorial disorder involving both motor and non-motor symptoms caused by the progressive death of distinct neuronal populations, including dopaminergic neurons in the substantia nigra. The deposition of aggregated α-synuclein protein into Lewy body inclusions is a hallmark of the disorder, and α-synuclein pathology has been found in the enteric nervous system (ENS) of PD patients up to two decades prior to diagnosis. In combination with the high occurrence of gastrointestinal dysfunction in early stages of PD, current evidence strongly suggests that some forms of PD may originate in the gut. In this review, we discuss human studies that support ENS Lewy pathology as a characteristic feature of PD, and present evidence from humans and animal model systems that α-synuclein aggregation may follow a prion-like spreading cascade from enteric neurons, through the vagal nerve, and into the brain. Given the accessibility of the human gut to pharmacologic and dietary interventions, therapeutic strategies aimed at reducing pathological α-synuclein in the gastrointestinal tract hold significant promise for PD treatment.

Scientific assessment

01

Research question

Assess the question within the original study’s scope.

02

Methods & sample

Check the source article for study design and sample details.

03

Key findings

An editorially approved findings summary is not yet published for this record.

04

Limitations

Generalizability, bias and clinical meaning require separate assessment.

Methods, samples and clinical conclusions are not inferred from bibliographic metadata.