Spreading of α-synuclein in the face of axonal transport deficits in Parkinson's disease: A speculative synthesis.
Författare
Summary, in English
Parkinson's disease (PD) is mainly attributed to degeneration of dopamine neurons in the substantia nigra, but its etiopathogenesis also includes impaired protein clearance and axonal transport dysfunction, among others. The spread of α-synuclein (α-syn) aggregates from one neuron to another, in a prion-like manner, is hypothesized to contribute to PD progression. Axonal transport is likely to play a crucial role in this movement of α-syn aggregates between brain regions. At the same time, deficits in axonal transport are suggested to contribute to neuronal failure in PD. In this review, we discuss the apparent contradiction that axonal transport might be essential for disease progression, while dysfunction of axonal transport could simultaneously be a cornerstone of PD pathogenesis. We speculate around models that reconcile how axonal transport can play such a paradoxical role.
Publiceringsår
2015
Språk
Engelska
Sidor
276-283
Publikation/Tidskrift/Serie
Neurobiology of Disease
Volym
77
Issue
Jul 15
Länkar
Dokumenttyp
Artikel i tidskrift
Förlag
Elsevier
Ämne
- Neurosciences
Status
Published
ISBN/ISSN/Övrigt
- ISSN: 0969-9961