期刊论文详细信息
Molecular Neurodegeneration
Alpha-synuclein and tau: teammates in neurodegeneration?
Pamela J McLean2  Owen A Ross2  Marion Delenclos1  Elisabeth L Moussaud-Lamodière1  Daryl R Jones1  Simon Moussaud1 
[1] Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA;Mayo Graduate School, Mayo Clinic College of Medicine, 200 1st St SW, Rochester, MN 55905, USA
关键词: Alzheimer’s disease;    Parkinson’s disease;    Tauopathy;    Synucleinopathy;    Tangles;    Oligomers;    SNCA;    Synuclein;    MAPT;    Tau;   
Others  :  1132686
DOI  :  10.1186/1750-1326-9-43
 received in 2014-04-03, accepted in 2014-10-16,  发布年份 2014
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【 摘 要 】

The accumulation of α-synuclein aggregates is the hallmark of Parkinson’s disease, and more generally of synucleinopathies. The accumulation of tau aggregates however is classically found in the brains of patients with dementia, and this type of neuropathological feature specifically defines the tauopathies. Nevertheless, in numerous cases α-synuclein positive inclusions are also described in tauopathies and vice versa, suggesting a co-existence or crosstalk of these proteinopathies. Interestingly, α-synuclein and tau share striking common characteristics suggesting that they may work in concord. Tau and α-synuclein are both partially unfolded proteins that can form toxic oligomers and abnormal intracellular aggregates under pathological conditions. Furthermore, mutations in either are responsible for severe dominant familial neurodegeneration. Moreover, tau and α-synuclein appear to promote the fibrillization and solubility of each other in vitro and in vivo. This suggests that interactions between tau and α-synuclein form a deleterious feed-forward loop essential for the development and spreading of neurodegeneration. Here, we review the recent literature with respect to elucidating the possible links between α-synuclein and tau.

【 授权许可】

   
2014 Moussaud et al.; licensee BioMed Central Ltd.

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