Departamento de Biología Celular y Molecular, Pontificia Universidad Católica de Chile, Santiago, Chile.
Curr Alzheimer Res. 2011 Sep;8(6):643-51. doi: 10.2174/156720511796717249.
Hyperphosphorylated tau is a cardinal feature of Alzheimer's disease (AD) pathology. The deregulation of kinases that phosphorylate tau can alter normal tau-related processes, including microtubule dynamics, growth cones, and axonal transport, and induce tau aggregation in paired helical filaments. Here we discuss the possible roles of the Abl family of tyrosine kinases, which are essential regulators of cytoskeleton cellular signaling cascades, in AD tau pathology and how the physiological roles of Abl kinases could be connected with the cytoskeletal alterations induced by Aβ aggregates and AD progression.
过度磷酸化的 tau 是阿尔茨海默病(AD)病理学的一个主要特征。磷酸化 tau 的激酶失调会改变正常的 tau 相关过程,包括微管动力学、生长锥和轴突运输,并诱导双螺旋丝中 tau 的聚集。在这里,我们讨论了 Abl 家族酪氨酸激酶在 AD tau 病理学中的可能作用,这些激酶是细胞骨架信号级联反应的重要调节剂,以及 Abl 激酶的生理作用如何与 Aβ 聚集和 AD 进展引起的细胞骨架改变相关。