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Related Experiment Video

Updated: Nov 2, 2025

A Method to Study α-Synuclein Toxicity and Aggregation Using a Humanized Yeast Model
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Polymyxin B accelerates the α-synuclein aggregation.

Anshuman Mohapatra1, Vijay Singh Bohara1, Sachin Kumar1

  • 1Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati 781 039, India.

Biophysical Chemistry
|June 12, 2021
PubMed
Summary

Polymyxin B, an antibiotic used for infections, appears to worsen Parkinson's disease (PD) by accelerating the formation of toxic alpha-synuclein protein clumps. This finding suggests a potential new therapeutic target for PD.

Keywords:
Alpha-synucleinAmyloidKineticsPolymyxin B

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Parkinson's disease (PD) is a neurodegenerative disorder linked to alpha-synuclein aggregation.
  • Constipation is a common PD symptom, and some antibiotics may improve PD. Polymyxin B, an antibiotic, alleviates PD motor symptoms, but its mechanism is unknown.

Purpose of the Study:

  • To investigate if Polymyxin B influences alpha-synuclein aggregation, a key pathological feature of Parkinson's disease.

Main Methods:

  • In vitro study of alpha-synuclein aggregation kinetics.
  • Assessing the effect of Polymyxin B on the lag phase of alpha-synuclein fibril formation.

Main Results:

  • Polymyxin B significantly catalyzes the aggregation of alpha-synuclein into amyloid fibrils.
  • The presence of Polymyxin B reduced the lag phase of aggregation by approximately two-thirds.

Conclusions:

  • Polymyxin B promotes alpha-synuclein aggregation, potentially explaining its effect on Parkinson's disease symptoms.
  • This interaction highlights a novel mechanism by which antibiotics might influence PD pathology and suggests therapeutic avenues.