Research output: Contribution to journal › Article › peer-review
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.Research output: Contribution to journal › Article › peer-review
}
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