In the case of AD, Heredia et al. showed that hippocampal neurons treated with fibrillar Aβ have increased levels of inactive Ser3 phosphorylated ADF/cofilin (an ADP-actin severing protein) and active Thr508 phosphorylated LIM kinase 1 (an ADF/cofilin inhibitor by phosphorylating Ser3), resulting in dramatic remodelling of actin filaments (actin filament accumulation) and neuronal degeneration [237]. The gene discussed is GSN; the disease is Alzheimer disease.