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Related Experiment Video

Updated: Feb 14, 2026

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo
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Release and uptake of pathologic alpha-synuclein.

Veselin Grozdanov1, Karin M Danzer2

  • 1Neurology, Ulm University, Ulm, Germany.

Cell and Tissue Research
|February 8, 2018
PubMed
Summary

Alpha-synuclein (α-syn) aggregation is central to Parkinson's disease (PD). This review explores how α-syn spreads between cells, a key process in PD pathology, and identifies unanswered questions regarding its release and uptake mechanisms.

Keywords:
Alpha synucleinCell-to-cell transmissionExosomesParkinson’s diseaseSpreading

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Parkinson's disease (PD) involves dopaminergic neuron loss and Lewy bodies, characterized by aggregated alpha-synuclein (α-syn).
  • Evidence strongly suggests α-syn aggregation is critical in PD and other synucleinopathies.
  • Pathology spread implies cell-to-cell transmission of α-syn.

Purpose of the Study:

  • To review the current understanding of α-syn release and uptake mechanisms.
  • To highlight the critical role of α-syn cell-to-cell transmission in PD.
  • To identify key unanswered questions in the field.

Main Methods:

  • Literature review of in vitro and in vivo studies on α-syn.
  • Analysis of evidence for α-syn release from and uptake into cells.
  • Discussion of proposed mechanisms for α-syn intercellular spread.

Main Results:

  • In vitro and in vivo studies confirm aggregation-prone α-syn can spread between cells.
  • Extracellular release and subsequent uptake by recipient cells are necessary for α-syn transmission.
  • Internalized α-syn must access the cytoplasm or target organelles.

Conclusions:

  • Cell-to-cell transmission of α-syn is a significant factor in Parkinson's disease progression.
  • The precise mechanisms of α-syn release, uptake, and intracellular trafficking remain incompletely understood.
  • Further research is needed to elucidate these pathways and their role in synucleinopathies.