Heredia, L., Helguera, P., de Olmos, S., Kedikian, G., Solá Vigo, F., LaFerla, F., Staufenbiel, M., De Olmos, J., Busciglio, J., Cáceres, A., & Lorenzo, A. (2006). Phosphorylation of Actin-Depolymerizing Factor/Cofilin by LIM-Kinase Mediates Amyloid Beta-Induced Degeneration: A Potential Mechanism of Neuronal Dystrophy in Alzheimer’s Disease. Journal of Neuroscience, 26, 6533-6542.
http://dx.doi.org/10.1523/JNEUROSCI.5567-05.2006

has been cited by the following article:

• TITLE: Roles of BMP6/7 in Actin Dynamics in Amyloid β-Induced Neurotoxicity

  AUTHORS: Lin Sun, Yingjie Zhang, Shifu Xiao

  KEYWORDS: Amyloid β, BMP, Actin Dynamics, LIMK1, Alzheimer’s Disease

  JOURNAL NAME: Psychology, Vol.5 No.7, May 22, 2014

  ABSTRACT: Actin dynamics plays an important role in many physiological functions such as long-term potentiation, neurotransmission, regulatory proteins translocation, ATP cycle, etc. When amyloid β (Aβ)-induced neurotoxicity occurs, the imbalance of actin dynamics leads to dystrophy of dendrites, which is characteristic pathology in Alzheimer’s disease (AD). Transient and persistent Aβ neurotoxicity provokes distinct manifestations of actin dynamics and causes opposing effects in AD. It has been shown that bone morphogenetic protein 6/7 (BMP6/7) protects neuronal morphology against Aβ-induced neurotoxicity, and can directly bind to LIM kinase1 (LIMK1), being one part of the upstream regulatory pathway of actin dynamics. This review aims to discuss a potential mechanism of BMPs underlying maintainance of cytoskeletal stabilization in neurite.