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A Genetic Mouse Model of Parkinson's Disease Shows Involuntary Movements and Increased Postsynaptic Sensitivity to Apomorphine.

Author: AuburgerG, BezF, BrehmN, CarlssonT, CenciM A, GispertS, KernB

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.

Overview

Alpha-synuclein aggregation causes Parkinson's disease. This study found that a genetic mouse model of early Parkinson's disease showed a disturbance in ERK1/2 signaling associated with apomorphine-induced involuntary movements. This model could help identify new therapies to address the abnormal dopamine-dependent striatal plasticity seen in Parkinson's disease.
Paper Details　
Original Abstract of the Article :
Alpha-synuclein (SNCA) protein aggregation plays a causal role in Parkinson's disease (PD). The SNCA protein modulates neurotransmission via the SNAP receptor (SNARE) complex assembly and presynaptic vesicle trafficking. The striatal presynaptic dopamine deficit is alleviated by treatment with levod...See full text at original site
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引用元：
https://doi.org/10.1007/s12035-014-8911-6

データ提供：米国国立医学図書館（NLM）

Parkinson's Disease: Unraveling the Mystery of Involuntary Movements

The quest to understand the mechanisms underlying [Parkinson's disease (PD)] continues, with a particular focus on the role of [alpha-synuclein (SNCA) protein aggregation]. This study investigates the postsynaptic supersensitivity to [apomorphine] in a genetic mouse model of early PD. Researchers examined the behavioral and molecular changes induced by apomorphine in mice overexpressing A53T-SNCA.

Apomorphine-Induced Involuntary Movements: A Deeper Understanding

The study demonstrates a greater sensitivity to apomorphine-induced involuntary movements in A53T-transgenic mice compared to wild-type controls. These findings provide valuable insights into the underlying mechanisms of dyskinesia in PD, highlighting the importance of postsynaptic dopamine receptor-mediated signaling in this complex condition.

Towards Effective PD Treatments: Targeting Postsynaptic Plasticity

The study emphasizes the crucial role of postsynaptic plasticity in PD, particularly in the development of dyskinesia. Understanding the complex interplay between dopamine receptors and downstream signaling pathways offers potential avenues for developing new therapeutic strategies that could effectively manage dyskinesia and improve the quality of life for individuals with PD.

Dr.Camel's Conclusion

Just like a camel navigating a desert with its unique adaptations, we must navigate the complexities of PD with innovative approaches. This study sheds light on the crucial role of postsynaptic supersensitivity in PD, opening doors for new therapeutic strategies that could help alleviate the debilitating symptoms of this devastating disease.

Date :
  1. Date Completed 2016-08-08
  2. Date Revised 2021-10-21
Further Info :

Pubmed ID

25307288

DOI: Digital Object Identifier

10.1007/s12035-014-8911-6

Related Literature

Article Analysis
・Effects of apomorphine injection
SNS
PICO Info
in preparation
Languages

English

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