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Malfunctions in synaptic membrane trafficking in early pathology of Parkinson´s disease: new molecular clues. / Sopova, Elena ; Korenkova, Olga ; Shupliakov, Oleg .

In: Biological Communications, Vol. 62, No. 4, 2018, p. 272-277.

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@article{8a48e0fdd6014c428739c90f3fa13794,
title = "Malfunctions in synaptic membrane trafficking in early pathology of Parkinson´s disease: new molecular clues.",
abstract = "The midbrain dopaminergic neurons of the substantia nigra and the ventral tegmental area play vital roles in the regulation of voluntary movement, emo-tion 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 syn-aptic connections fail, humans develop Parkinson´s disease. This disease is ac-companied by the accumulation of toxic α-synuclein-containing protein aggre-gates 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 traffickinin the nerve terminal and the au-tophagy–lysosomal pathway is the site for the aggregate assembly. An urgent goal is to findtherapeutic targets at early stages of the disease when neurons are still functional.",
keywords = "synapse, synaptic proteins, atophagy-lysosomal pathway, develop-mental transcription factors, Parkinson´s disease",
author = "Elena Sopova and Olga Korenkova and Oleg Shupliakov",
year = "2018",
doi = "10.21638/11701/spbu03.2017.406",
language = "English",
volume = "62",
pages = "272--277",
journal = "Biological Communications",
issn = "2542-2154",
publisher = "Издательство Санкт-Петербургского университета",
number = "4",

}

RIS

TY - JOUR

T1 - Malfunctions in synaptic membrane trafficking in early pathology of Parkinson´s disease: new molecular clues.

AU - Sopova, Elena

AU - Korenkova, Olga

AU - Shupliakov, Oleg

PY - 2018

Y1 - 2018

N2 - The midbrain dopaminergic neurons of the substantia nigra and the ventral tegmental area play vital roles in the regulation of voluntary movement, emo-tion 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 syn-aptic connections fail, humans develop Parkinson´s disease. This disease is ac-companied by the accumulation of toxic α-synuclein-containing protein aggre-gates 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 traffickinin the nerve terminal and the au-tophagy–lysosomal pathway is the site for the aggregate assembly. An urgent goal is to findtherapeutic targets at early stages of the disease when neurons are still functional.

AB - The midbrain dopaminergic neurons of the substantia nigra and the ventral tegmental area play vital roles in the regulation of voluntary movement, emo-tion 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 syn-aptic connections fail, humans develop Parkinson´s disease. This disease is ac-companied by the accumulation of toxic α-synuclein-containing protein aggre-gates 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 traffickinin the nerve terminal and the au-tophagy–lysosomal pathway is the site for the aggregate assembly. An urgent goal is to findtherapeutic targets at early stages of the disease when neurons are still functional.

KW - synapse, synaptic proteins, atophagy-lysosomal pathway, develop-mental transcription factors, Parkinson´s disease

U2 - 10.21638/11701/spbu03.2017.406

DO - 10.21638/11701/spbu03.2017.406

M3 - Article

VL - 62

SP - 272

EP - 277

JO - Biological Communications

JF - Biological Communications

SN - 2542-2154

IS - 4

ER -

ID: 16798228