Neural Regeneration Research ›› 2024, Vol. 19 ›› Issue (12): 2581-2582.doi: 10.4103/NRR.NRR-D-23-01900

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Strain-dependent alpha-synuclein spreading in Parkinson’s disease and multiple system atrophy

Shuyu Zhang, Paul Lingor*   

  1. Department of Neurology, School of Medicine, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany (Zhang S, Lingor P) 
    Department of Neurology, University Medical Center Göttingen, Göttingen, Germany (Lingor P) 
    Center for Biostructural Imaging of Neurodegeneration, University Medical Center Göttingen, Göttingen, Germany (Lingor P)
  • Online:2024-12-15 Published:2024-03-30
  • Contact: Paul Lingor, MD, paul.lingor@tum.de.
  • Supported by:
    This work was supported by Deutsche Forschungsgemeinschaft, EXC 2145 SyNergy, Grant No. 390857198 (to PL).

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Abstract: Parkinson’s disease (PD) and atypical Parkinsonian syndromes, such as multiple system atrophy (MSA) and Dementia with Lewy bodies, are neurodegenerative movement disorders characterized by the accumulation of alpha-synuclein (α-syn) aggregates. These α-syn aggregates propagate throughout the brain in a prion-like manner, where pathological α-syn recruits endogenous α-syn to form insoluble aggregates. Oligomeric forms representing intermediates on the way to insoluble aggregates result in the most pronounced neurotoxic effects. α-Syn aggregates can further assemble into Lewy bodies (LB) in PD and glial cytoplasmatic inclusions (GCI) in MSA, leading to neuronal dysfunction and degeneration.