摘要
突轴核蛋白 (α synuclein)是一种存在于突触前膜的蛋白 ,具有调节突触可塑性等正常生理功能。但其大量的积聚和变异将引起神经细胞的损伤 ,以致引起许多神经退行性疾病。在此过程中 ,α synuclein聚集和与其他分子相互作用的性质可能是关键因素。研究发现α synuclein是阿尔采末病人的老年斑块中非Aβ蛋白组分的前体 ,表明α synuclein的异常可能与阿尔采末病的病理过程有密切的关系。该文就其近年的研究进展做一综述。
syuclein is regarded as a presynaptic protein, which may play an important role in neuronal plasticity. However, abnormal accumulation of fibrillar α-synuclein and mutation of α-synuclein gene can affect the survival of neurons. Its aggregation and interaction with other proteins are the most critical factors. α-synuclein is a precursor of non-amyloid component of senile plaques in Alzheimers disease. It is likely that α-synuclein is associated with Alzheimers pathology. In this paper, we summarize the progress in the normal physical function of α-synuclein and the mechanism in Alzheimers disease.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2004年第7期721-725,共5页
Chinese Pharmacological Bulletin