title: Malfunctions in synaptic membrane trafficking in early pathology of Parkinson’s disease: New molecular clues
metadata.name: dc.contributor.author
metadata.value: Sopova, Elena
metadata.lang: -
metadata.name: dc.contributor.author
metadata.value: Korenkova, Olga
metadata.lang: -
metadata.name: dc.contributor.author
metadata.value: Shupliakov, Oleg
metadata.lang: -
metadata.name: dc.date.accessioned
metadata.value: 2018-06-06T09:30:05Z
metadata.lang: -
metadata.name: dc.date.available
metadata.value: 2018-06-06T09:30:05Z
metadata.lang: -
metadata.name: dc.date.issued
metadata.value: 2017-12
metadata.lang: -
metadata.name: dc.identifier.citation
metadata.value: Sopova, E., Korenkova, O., and Shupliakov, O. 2017. Malfunctions in synaptic membrane trafficking in early pathology of Parkinson´s disease: New molecular clues. Bio. Comm. 62(4): 272–277.
metadata.lang: en_GB
metadata.name: dc.identifier.other
metadata.value: 10.21638/11701/ spbu03.2017.406
metadata.lang: -
metadata.name: dc.identifier.uri
metadata.value: http://hdl.handle.net/11701/10261
metadata.lang: -
metadata.name: dc.description.abstract
metadata.value: The midbrain dopaminergic neurons of the substantia nigra and the ventral
  tegmental area play vital roles in the regulation of voluntary movement, emotion
  and reward in humans. These neurons are highly metabolic and are under
  constant oxidative stress. The dopaminergic neurons form extensive synaptic
  projections to the striatum. When these neurons start dying or when their synaptic
  connections fail, humans develop Parkinson´s disease. This disease is accompanied
  by the accumulation of toxic α-synuclein-containing protein aggregates
  in nigrostriatal processes. Synucleins accumulate in a majority of healthy
  nerve terminals in the central nervous system, but what causes the formation
  of pathological synuclein aggregates is unclear. Recent studies point out that
  the interface between membrane trafficking in the nerve terminal and the autophagy–
  lysosomal pathway is the site for the aggregate assembly. An urgent
  goal is to find therapeutic targets at early stages of the disease when neurons
  are still functional.
metadata.lang: en_GB
metadata.name: dc.description.sponsorship
metadata.value: This work was supported by
  the Russian Science Foundation (Grant
  No. 16‑15-10273), the Swedish Medical
  Research Council (Grant No. VR-M №1501),
  and Parkinsonfonden.
metadata.lang: en_GB
metadata.name: dc.language.iso
metadata.value: en
metadata.lang: en_GB
metadata.name: dc.publisher
metadata.value: St Petersburg State University
metadata.lang: en_GB
metadata.name: dc.relation.ispartofseries
metadata.value: Biological Communications;Volume 62; Issue 4
metadata.lang: -
metadata.name: dc.subject
metadata.value: synapse
metadata.lang: en_GB
metadata.name: dc.subject
metadata.value: synaptic proteins
metadata.lang: en_GB
metadata.name: dc.subject
metadata.value: atophagy-lysosomal pathway
metadata.lang: en_GB
metadata.name: dc.subject
metadata.value: developmental transcription factors
metadata.lang: en_GB
metadata.name: dc.subject
metadata.value: Parkinson´s disease
metadata.lang: en_GB
metadata.name: dc.title
metadata.value: Malfunctions in synaptic membrane trafficking in early pathology of Parkinson’s disease: New molecular clues
metadata.lang: en_GB
metadata.name: dc.type
metadata.value: Article
metadata.lang: en_GB
resources.filename: 06-Sopova.pdf
resources.url: https://dspace.spbu.ru/bitstream/11701/10261/1/06-Sopova.pdf
resources.format: Adobe PDF
resources.size: 862,06 kB