Spreading of α-synuclein in the face of axonal transport deficits in Parkinson's disease: A speculative synthesis.

Research output: Contribution to journalReview article

Abstract

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.

Details

Authors
  • Jennifer T Lamberts
  • Erin Hildebrandt
  • Patrik Brundin
Organisations
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Neurosciences
Original languageEnglish
Pages (from-to)276-283
JournalNeurobiology of Disease
Volume77
Issue numberJul 15
Publication statusPublished - 2015
Publication categoryResearch
Peer-reviewedYes