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Related Experiment Video

Updated: Oct 10, 2025

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

Published on: June 2, 2019

Differentially targeted seeding reveals unique pathological alpha-synuclein propagation patterns.

Shady Rahayel^1,2, Bratislav Mišić¹, Ying-Qiu Zheng³

¹Department of Neurology and Neurosurgery, The Neuro (Montreal Neurological Institute-Hospital), Montreal, Quebec H3A 2B4, Canada.

Brain : a Journal of Neurology

|December 15, 2021

Summary

This summary is machine-generated.

This study tracked the spread of alpha-synuclein pathology in mice over 24 months, revealing that normal alpha-synuclein levels and brain connectivity influence disease progression, supporting a prion-like spread model.

Keywords:

Snca Parkinson’s disease alpha-synuclein modelling synucleinopathy

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Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

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Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

Related Experiment Videos

Last Updated: Oct 10, 2025

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

Published on: June 2, 2019

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

Published on: December 8, 2015

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

Area of Science:

Neuroscience
Computational Biology
Pathology

Background:

Parkinson's disease is a neurodegenerative disorder marked by alpha-synuclein aggregation.
The spread of pathologic alpha-synuclein through neuronal networks is implicated in disease progression.
Mechanisms of abnormal protein propagation in the brain remain incompletely understood.

Purpose of the Study:

To map the long-term spatiotemporal distribution of Lewy-related pathology in mice.
To develop a computational model simulating the spread of pathologic alpha-synuclein.
To investigate factors influencing alpha-synuclein propagation patterns.

Main Methods:

Injected alpha-synuclein preformed fibrils into 87 mice across specific brain regions.
Quantified hyperphosphorylated alpha-synuclein pathology over 24 months at seven time points.
Utilized a Susceptible-Infected-Removed (SIR) computational model incorporating brain connectivity and gene expression.

Main Results:

Differential seeding of alpha-synuclein resulted in unique propagation patterns over 24 months.
Most brain regions were found to be permissive to pathology.
The SIR model accurately recreated observed pathology distributions, with Snca gene expression and connectivity significantly influencing model fit.

Conclusions:

Normal alpha-synuclein concentration and brain connectomics increase regional vulnerability to pathology.
Findings support a prion-like spread mechanism for pathologic alpha-synuclein.
The developed dataset and model can facilitate research into factors altering alpha-synuclein spread.