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

Lamberts, Jennifer T; Hildebrandt, Erin and Brundin, Patrik LU (2015) In Neurobiology of Disease 77(Jul 15). p.276-283
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Neurobiology of Disease
volume
77
issue
Jul 15
pages
276 - 283
publisher
Elsevier
external identifiers
  • pmid:25046996
  • wos:000353612200025
  • scopus:84927598926
ISSN
0969-9961
DOI
10.1016/j.nbd.2014.07.002
language
English
LU publication?
yes
id
9be8ee5d-3dde-4f06-bf3e-d400e96483e9 (old id 4581561)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25046996?dopt=Abstract
date added to LUP
2014-08-08 23:49:07
date last changed
2017-10-22 03:14:50
@article{9be8ee5d-3dde-4f06-bf3e-d400e96483e9,
  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.},
  author       = {Lamberts, Jennifer T and Hildebrandt, Erin and Brundin, Patrik},
  issn         = {0969-9961},
  language     = {eng},
  number       = {Jul 15},
  pages        = {276--283},
  publisher    = {Elsevier},
  series       = {Neurobiology of Disease},
  title        = {Spreading of α-synuclein in the face of axonal transport deficits in Parkinson's disease: A speculative synthesis.},
  url          = {http://dx.doi.org/10.1016/j.nbd.2014.07.002},
  volume       = {77},
  year         = {2015},
}